Reactive Oxygen Species: Drivers of Physiological and Pathological Processes
Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigaci&...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Checa J [verfasserIn] Aran JM [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2020 |
|---|
| Schlagwörter: |
|---|
| Übergeordnetes Werk: |
In: Journal of Inflammation Research - Dove Medical Press, 2009, (2020), Seite 1057-1073 |
|---|---|
| Übergeordnetes Werk: |
year:2020 ; pages:1057-1073 |
| Links: |
|---|
| Katalog-ID: |
DOAJ059881097 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | DOAJ059881097 | ||
| 003 | DE-627 | ||
| 005 | 20230502074129.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 230228s2020 xx |||||o 00| ||eng c | ||
| 035 | |a (DE-627)DOAJ059881097 | ||
| 035 | |a (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 050 | 0 | |a RB1-214 | |
| 050 | 0 | |a RM1-950 | |
| 100 | 0 | |a Checa J |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| 264 | 1 | |c 2020 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation | ||
| 650 | 4 | |a reactive oxygen species | |
| 650 | 4 | |a oxidative stress | |
| 650 | 4 | |a inflammation. | |
| 653 | 0 | |a Pathology | |
| 653 | 0 | |a Therapeutics. Pharmacology | |
| 700 | 0 | |a Aran JM |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i In |t Journal of Inflammation Research |d Dove Medical Press, 2009 |g (2020), Seite 1057-1073 |w (DE-627)600306178 |w (DE-600)2494878-0 |x 11787031 |7 nnns |
| 773 | 1 | 8 | |g year:2020 |g pages:1057-1073 |
| 856 | 4 | 0 | |u https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 |z kostenfrei |
| 856 | 4 | 0 | |u https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR |z kostenfrei |
| 856 | 4 | 2 | |u https://doaj.org/toc/1178-7031 |y Journal toc |z kostenfrei |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a SYSFLAG_A | ||
| 912 | |a GBV_DOAJ | ||
| 912 | |a SSG-OLC-PHA | ||
| 912 | |a GBV_ILN_11 | ||
| 912 | |a GBV_ILN_20 | ||
| 912 | |a GBV_ILN_22 | ||
| 912 | |a GBV_ILN_23 | ||
| 912 | |a GBV_ILN_24 | ||
| 912 | |a GBV_ILN_39 | ||
| 912 | |a GBV_ILN_40 | ||
| 912 | |a GBV_ILN_60 | ||
| 912 | |a GBV_ILN_62 | ||
| 912 | |a GBV_ILN_63 | ||
| 912 | |a GBV_ILN_65 | ||
| 912 | |a GBV_ILN_69 | ||
| 912 | |a GBV_ILN_73 | ||
| 912 | |a GBV_ILN_74 | ||
| 912 | |a GBV_ILN_95 | ||
| 912 | |a GBV_ILN_105 | ||
| 912 | |a GBV_ILN_110 | ||
| 912 | |a GBV_ILN_151 | ||
| 912 | |a GBV_ILN_161 | ||
| 912 | |a GBV_ILN_170 | ||
| 912 | |a GBV_ILN_206 | ||
| 912 | |a GBV_ILN_213 | ||
| 912 | |a GBV_ILN_230 | ||
| 912 | |a GBV_ILN_285 | ||
| 912 | |a GBV_ILN_293 | ||
| 912 | |a GBV_ILN_602 | ||
| 912 | |a GBV_ILN_2003 | ||
| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_4012 | ||
| 912 | |a GBV_ILN_4037 | ||
| 912 | |a GBV_ILN_4112 | ||
| 912 | |a GBV_ILN_4125 | ||
| 912 | |a GBV_ILN_4126 | ||
| 912 | |a GBV_ILN_4249 | ||
| 912 | |a GBV_ILN_4305 | ||
| 912 | |a GBV_ILN_4306 | ||
| 912 | |a GBV_ILN_4307 | ||
| 912 | |a GBV_ILN_4313 | ||
| 912 | |a GBV_ILN_4322 | ||
| 912 | |a GBV_ILN_4323 | ||
| 912 | |a GBV_ILN_4324 | ||
| 912 | |a GBV_ILN_4325 | ||
| 912 | |a GBV_ILN_4338 | ||
| 912 | |a GBV_ILN_4367 | ||
| 912 | |a GBV_ILN_4700 | ||
| 951 | |a AR | ||
| 952 | |j 2020 |h 1057-1073 | ||
| author_variant |
c j cj a j aj |
|---|---|
| matchkey_str |
article:11787031:2020----::eciexgnpcediesfhsooiaada |
| hierarchy_sort_str |
2020 |
| callnumber-subject-code |
RB |
| publishDate |
2020 |
| allfields |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Checa J verfasserin aut Reactive Oxygen Species: Drivers of Physiological and Pathological Processes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology Aran JM verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2020), Seite 1057-1073 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2020 pages:1057-1073 https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 kostenfrei https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 1057-1073 |
| spelling |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Checa J verfasserin aut Reactive Oxygen Species: Drivers of Physiological and Pathological Processes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology Aran JM verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2020), Seite 1057-1073 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2020 pages:1057-1073 https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 kostenfrei https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 1057-1073 |
| allfields_unstemmed |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Checa J verfasserin aut Reactive Oxygen Species: Drivers of Physiological and Pathological Processes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology Aran JM verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2020), Seite 1057-1073 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2020 pages:1057-1073 https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 kostenfrei https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 1057-1073 |
| allfieldsGer |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Checa J verfasserin aut Reactive Oxygen Species: Drivers of Physiological and Pathological Processes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology Aran JM verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2020), Seite 1057-1073 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2020 pages:1057-1073 https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 kostenfrei https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 1057-1073 |
| allfieldsSound |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Checa J verfasserin aut Reactive Oxygen Species: Drivers of Physiological and Pathological Processes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology Aran JM verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2020), Seite 1057-1073 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2020 pages:1057-1073 https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 kostenfrei https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 1057-1073 |
| language |
English |
| source |
In Journal of Inflammation Research (2020), Seite 1057-1073 year:2020 pages:1057-1073 |
| sourceStr |
In Journal of Inflammation Research (2020), Seite 1057-1073 year:2020 pages:1057-1073 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
reactive oxygen species oxidative stress inflammation. Pathology Therapeutics. Pharmacology |
| isfreeaccess_bool |
true |
| container_title |
Journal of Inflammation Research |
| authorswithroles_txt_mv |
Checa J @@aut@@ Aran JM @@aut@@ |
| publishDateDaySort_date |
2020-01-01T00:00:00Z |
| hierarchy_top_id |
600306178 |
| id |
DOAJ059881097 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ059881097</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502074129.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2020 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ059881097</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RB1-214</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RM1-950</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Checa J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Reactive Oxygen Species: Drivers of Physiological and Pathological Processes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L&rsquo;Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d&rsquo;Investigaci&oacute; Biom&egrave;dica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L&rsquo;Hospitalet de Llobregat, Gran V&iacute;a de L&rsquo;Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism&rsquo;s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NF&kappa;B/I&kappa;B, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">reactive oxygen species</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">oxidative stress</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammation.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Pathology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Therapeutics. Pharmacology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Aran JM</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of Inflammation Research</subfield><subfield code="d">Dove Medical Press, 2009</subfield><subfield code="g">(2020), Seite 1057-1073</subfield><subfield code="w">(DE-627)600306178</subfield><subfield code="w">(DE-600)2494878-0</subfield><subfield code="x">11787031</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">year:2020</subfield><subfield code="g">pages:1057-1073</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1178-7031</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="j">2020</subfield><subfield code="h">1057-1073</subfield></datafield></record></collection>
|
| callnumber-first |
R - Medicine |
| author |
Checa J |
| spellingShingle |
Checa J misc RB1-214 misc RM1-950 misc reactive oxygen species misc oxidative stress misc inflammation. misc Pathology misc Therapeutics. Pharmacology Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| authorStr |
Checa J |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)600306178 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut |
| collection |
DOAJ |
| remote_str |
true |
| callnumber-label |
RB1-214 |
| illustrated |
Not Illustrated |
| issn |
11787031 |
| topic_title |
RB1-214 RM1-950 Reactive Oxygen Species: Drivers of Physiological and Pathological Processes reactive oxygen species oxidative stress inflammation |
| topic |
misc RB1-214 misc RM1-950 misc reactive oxygen species misc oxidative stress misc inflammation. misc Pathology misc Therapeutics. Pharmacology |
| topic_unstemmed |
misc RB1-214 misc RM1-950 misc reactive oxygen species misc oxidative stress misc inflammation. misc Pathology misc Therapeutics. Pharmacology |
| topic_browse |
misc RB1-214 misc RM1-950 misc reactive oxygen species misc oxidative stress misc inflammation. misc Pathology misc Therapeutics. Pharmacology |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
cr |
| hierarchy_parent_title |
Journal of Inflammation Research |
| hierarchy_parent_id |
600306178 |
| hierarchy_top_title |
Journal of Inflammation Research |
| isfreeaccess_txt |
true |
| familylinks_str_mv |
(DE-627)600306178 (DE-600)2494878-0 |
| title |
Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| ctrlnum |
(DE-627)DOAJ059881097 (DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4 |
| title_full |
Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| author_sort |
Checa J |
| journal |
Journal of Inflammation Research |
| journalStr |
Journal of Inflammation Research |
| callnumber-first-code |
R |
| lang_code |
eng |
| isOA_bool |
true |
| recordtype |
marc |
| publishDateSort |
2020 |
| contenttype_str_mv |
txt |
| container_start_page |
1057 |
| author_browse |
Checa J Aran JM |
| class |
RB1-214 RM1-950 |
| format_se |
Elektronische Aufsätze |
| author-letter |
Checa J |
| author2-role |
verfasserin |
| title_sort |
reactive oxygen species: drivers of physiological and pathological processes |
| callnumber |
RB1-214 |
| title_auth |
Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| abstract |
Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation |
| abstractGer |
Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation |
| abstract_unstemmed |
Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L’Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L’Hospitalet de Llobregat, Gran Vía de L’Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism’s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation |
| collection_details |
GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 |
| title_short |
Reactive Oxygen Species: Drivers of Physiological and Pathological Processes |
| url |
https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4 https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR https://doaj.org/toc/1178-7031 |
| remote_bool |
true |
| author2 |
Aran JM |
| author2Str |
Aran JM |
| ppnlink |
600306178 |
| callnumber-subject |
RB - Pathology |
| mediatype_str_mv |
c |
| isOA_txt |
true |
| hochschulschrift_bool |
false |
| callnumber-a |
RB1-214 |
| up_date |
2024-07-04T01:16:01.754Z |
| _version_ |
1803609190441156608 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ059881097</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502074129.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2020 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ059881097</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ2c5799753c744759ba0adb36c4bc88b4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RB1-214</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RM1-950</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Checa J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Reactive Oxygen Species: Drivers of Physiological and Pathological Processes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Javier Checa, Josep M Aran Immune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L&rsquo;Hospitalet de Llobregat, Barcelona 08907, SpainCorrespondence: Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, Institut d&rsquo;Investigaci&oacute; Biom&egrave;dica de Bellvitge (IDIBELL), Hospital Duran i Reynals, L&rsquo;Hospitalet de Llobregat, Gran V&iacute;a de L&rsquo;Hospitalet, 199, Barcelona 08908, SpainTel +34 93 2607428Fax +34 93 2607414Email jaranidibell.catAbstract: Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism&rsquo;s lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NF&kappa;B/I&kappa;B, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.Keywords: reactive oxygen species, oxidative stress, inflammation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">reactive oxygen species</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">oxidative stress</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammation.</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Pathology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Therapeutics. Pharmacology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Aran JM</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Journal of Inflammation Research</subfield><subfield code="d">Dove Medical Press, 2009</subfield><subfield code="g">(2020), Seite 1057-1073</subfield><subfield code="w">(DE-627)600306178</subfield><subfield code="w">(DE-600)2494878-0</subfield><subfield code="x">11787031</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">year:2020</subfield><subfield code="g">pages:1057-1073</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/2c5799753c744759ba0adb36c4bc88b4</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.dovepress.com/reactive-oxygen-species-drivers-of-physiological-and-pathological-proc-peer-reviewed-article-JIR</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1178-7031</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="j">2020</subfield><subfield code="h">1057-1073</subfield></datafield></record></collection>
|
| score |
7.4019136 |