Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction
Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory tr...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
He, Weixin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Inflammation research - Cham : Springer International Publishing AG, 1969, 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 |
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| Übergeordnetes Werk: |
volume:71 ; year:2022 ; number:10-11 ; day:25 ; month:07 ; pages:1143-1158 |
| Links: |
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| DOI / URN: |
10.1007/s00011-022-01611-0 |
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SPR048479039 |
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| 520 | |a Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. | ||
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| 650 | 4 | |a Myocardial infarction |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Chen, Qingquan |4 aut | |
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10.1007/s00011-022-01611-0 doi (DE-627)SPR048479039 (SPR)s00011-022-01611-0-e DE-627 ger DE-627 rakwb eng He, Weixin verfasserin aut Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. Cytokine storm (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Collateral circulation (dpeaa)DE-He213 Myocardial infarction (dpeaa)DE-He213 Coronary artery (dpeaa)DE-He213 Chen, Peixian aut Chen, Qingquan aut Cai, Zongtong aut Zhang, Peidong (orcid)0000-0003-3243-691X aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:71 year:2022 number:10-11 day:25 month:07 pages:1143-1158 https://dx.doi.org/10.1007/s00011-022-01611-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2022 10-11 25 07 1143-1158 |
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10.1007/s00011-022-01611-0 doi (DE-627)SPR048479039 (SPR)s00011-022-01611-0-e DE-627 ger DE-627 rakwb eng He, Weixin verfasserin aut Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. Cytokine storm (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Collateral circulation (dpeaa)DE-He213 Myocardial infarction (dpeaa)DE-He213 Coronary artery (dpeaa)DE-He213 Chen, Peixian aut Chen, Qingquan aut Cai, Zongtong aut Zhang, Peidong (orcid)0000-0003-3243-691X aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:71 year:2022 number:10-11 day:25 month:07 pages:1143-1158 https://dx.doi.org/10.1007/s00011-022-01611-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2022 10-11 25 07 1143-1158 |
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10.1007/s00011-022-01611-0 doi (DE-627)SPR048479039 (SPR)s00011-022-01611-0-e DE-627 ger DE-627 rakwb eng He, Weixin verfasserin aut Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. Cytokine storm (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Collateral circulation (dpeaa)DE-He213 Myocardial infarction (dpeaa)DE-He213 Coronary artery (dpeaa)DE-He213 Chen, Peixian aut Chen, Qingquan aut Cai, Zongtong aut Zhang, Peidong (orcid)0000-0003-3243-691X aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:71 year:2022 number:10-11 day:25 month:07 pages:1143-1158 https://dx.doi.org/10.1007/s00011-022-01611-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2022 10-11 25 07 1143-1158 |
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10.1007/s00011-022-01611-0 doi (DE-627)SPR048479039 (SPR)s00011-022-01611-0-e DE-627 ger DE-627 rakwb eng He, Weixin verfasserin aut Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. Cytokine storm (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Collateral circulation (dpeaa)DE-He213 Myocardial infarction (dpeaa)DE-He213 Coronary artery (dpeaa)DE-He213 Chen, Peixian aut Chen, Qingquan aut Cai, Zongtong aut Zhang, Peidong (orcid)0000-0003-3243-691X aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:71 year:2022 number:10-11 day:25 month:07 pages:1143-1158 https://dx.doi.org/10.1007/s00011-022-01611-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2022 10-11 25 07 1143-1158 |
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10.1007/s00011-022-01611-0 doi (DE-627)SPR048479039 (SPR)s00011-022-01611-0-e DE-627 ger DE-627 rakwb eng He, Weixin verfasserin aut Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. Cytokine storm (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Collateral circulation (dpeaa)DE-He213 Myocardial infarction (dpeaa)DE-He213 Coronary artery (dpeaa)DE-He213 Chen, Peixian aut Chen, Qingquan aut Cai, Zongtong aut Zhang, Peidong (orcid)0000-0003-3243-691X aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 71(2022), 10-11 vom: 25. Juli, Seite 1143-1158 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:71 year:2022 number:10-11 day:25 month:07 pages:1143-1158 https://dx.doi.org/10.1007/s00011-022-01611-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2022 10-11 25 07 1143-1158 |
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Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. 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cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction |
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Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction |
| abstract |
Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Abstract At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword “acute myocardial infarction”, “coronary collateral circulation” and “cytokine storm”, to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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10-11 |
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Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction |
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https://dx.doi.org/10.1007/s00011-022-01611-0 |
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Chen, Peixian Chen, Qingquan Cai, Zongtong Zhang, Peidong |
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Chen, Peixian Chen, Qingquan Cai, Zongtong Zhang, Peidong |
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10.1007/s00011-022-01611-0 |
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2024-07-03T19:28:52.294Z |
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| score |
7.4003115 |