Reactive oxygen species as signaling molecules in the development of lung fibrosis
Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia...
Ausführliche Beschreibung
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| Autor*in: |
Gonzalez-Gonzalez, Francisco J. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties - Muthuraja, A. ELSEVIER, 2015, the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research, New York, NY |
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| Übergeordnetes Werk: |
volume:190 ; year:2017 ; pages:61-68 ; extent:8 |
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| DOI / URN: |
10.1016/j.trsl.2017.09.005 |
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| 520 | |a Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. | ||
| 520 | |a Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. | ||
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| 700 | 1 | |a Budinger, G.R. Scott |4 oth | |
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10.1016/j.trsl.2017.09.005 doi GBV00000000000261A.pica (DE-627)ELV041157907 (ELSEVIER)S1931-5244(17)30278-5 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Gonzalez-Gonzalez, Francisco J. verfasserin aut Reactive oxygen species as signaling molecules in the development of lung fibrosis 2017transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. NADPH Elsevier TGF-β Elsevier Chandel, Navdeep S. oth Jain, Manu oth Budinger, G.R. Scott oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:190 year:2017 pages:61-68 extent:8 https://doi.org/10.1016/j.trsl.2017.09.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 190 2017 61-68 8 045F 610 |
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10.1016/j.trsl.2017.09.005 doi GBV00000000000261A.pica (DE-627)ELV041157907 (ELSEVIER)S1931-5244(17)30278-5 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Gonzalez-Gonzalez, Francisco J. verfasserin aut Reactive oxygen species as signaling molecules in the development of lung fibrosis 2017transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. NADPH Elsevier TGF-β Elsevier Chandel, Navdeep S. oth Jain, Manu oth Budinger, G.R. Scott oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:190 year:2017 pages:61-68 extent:8 https://doi.org/10.1016/j.trsl.2017.09.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 190 2017 61-68 8 045F 610 |
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10.1016/j.trsl.2017.09.005 doi GBV00000000000261A.pica (DE-627)ELV041157907 (ELSEVIER)S1931-5244(17)30278-5 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Gonzalez-Gonzalez, Francisco J. verfasserin aut Reactive oxygen species as signaling molecules in the development of lung fibrosis 2017transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. NADPH Elsevier TGF-β Elsevier Chandel, Navdeep S. oth Jain, Manu oth Budinger, G.R. Scott oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:190 year:2017 pages:61-68 extent:8 https://doi.org/10.1016/j.trsl.2017.09.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 190 2017 61-68 8 045F 610 |
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10.1016/j.trsl.2017.09.005 doi GBV00000000000261A.pica (DE-627)ELV041157907 (ELSEVIER)S1931-5244(17)30278-5 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Gonzalez-Gonzalez, Francisco J. verfasserin aut Reactive oxygen species as signaling molecules in the development of lung fibrosis 2017transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. NADPH Elsevier TGF-β Elsevier Chandel, Navdeep S. oth Jain, Manu oth Budinger, G.R. Scott oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:190 year:2017 pages:61-68 extent:8 https://doi.org/10.1016/j.trsl.2017.09.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 190 2017 61-68 8 045F 610 |
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10.1016/j.trsl.2017.09.005 doi GBV00000000000261A.pica (DE-627)ELV041157907 (ELSEVIER)S1931-5244(17)30278-5 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Gonzalez-Gonzalez, Francisco J. verfasserin aut Reactive oxygen species as signaling molecules in the development of lung fibrosis 2017transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. NADPH Elsevier TGF-β Elsevier Chandel, Navdeep S. oth Jain, Manu oth Budinger, G.R. Scott oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:190 year:2017 pages:61-68 extent:8 https://doi.org/10.1016/j.trsl.2017.09.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 190 2017 61-68 8 045F 610 |
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Enthalten in Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties New York, NY volume:190 year:2017 pages:61-68 extent:8 |
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Enthalten in Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties New York, NY volume:190 year:2017 pages:61-68 extent:8 |
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Reactive oxygen species as signaling molecules in the development of lung fibrosis |
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Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. |
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Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. |
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Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis. This epithelial injury leads to the activation and proliferation of myofibroblasts that secrete extracellular matrix proteins characteristic of fibrosis. The best described molecular link between alveolar epithelial dysfunction and myofibroblast activation and proliferation is the profibrotic cytokine transforming growth factor-β (TGF-β). We and others have found that mitochondrial and NAD(P)H oxidase-generated reactive oxygen species (ROS) play a signaling role to enhance TGF-β signaling and promote fibrosis. The purpose of this article is to review how ROS signaling leads to the activation of TGF-β. We suggest that an improved understanding of these pathways might explain the failure of nonselective antioxidants to improve outcomes in patients with pulmonary fibrosis and might identify novel targets for therapy. |
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