Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved..
The present review summarizes the beneficial and detrimental roles of reactive oxygen species in myocardial ischemia/reperfusion injury and cardioprotection. In the first part, the continued need for cardioprotection beyond that by rapid reperfusion of acute myocardial infarction is emphasized. Then, pathomechanisms of myocardial ischemia/reperfusion to the myocardium and the coronary circulation and the different modes of cell death in myocardial infarction are characterized. Different mechanical and pharmacological interventions to protect the ischemic/reperfused myocardium in elective percutaneous coronary interventions and coronary artery bypass grafting, in acute myocardial infarction and in cardiotoxicity from cancer therapy are detailed. The second part keeps the focus on ROS providing a comprehensive overview of molecular and cellular mechanisms involved in ischemia/reperfusion injury. Starting from mitochondria as the main sources and targets of ROS in ischemic/reperfused myocardium, a complex network of cellular and extracellular processes is discussed, including relationships with Ca2+ homeostasis, thiol group redox balance, hydrogen sulfide modulation, cross-talk with NAPDH oxidases, exosomes, cytokines and growth factors. While mechanistic insights are needed to improve our current therapeutic approaches, advancements in knowledge of ROS-mediated processes indicate that detrimental facets of oxidative stress are opposed by ROS requirement for physiological and protective reactions. This inevitable contrast is likely to underlie unsuccessful clinical trials and limits the development of novel cardioprotective interventions simply based upon ROS removal.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:67 |
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| Enthalten in: |
Redox biology - 67(2023) vom: 11. Nov., Seite 102894 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Heusch, Gerd [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 30.10.2023 Date Revised 13.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.redox.2023.102894 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM363322221 |
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| 500 | |a Date Revised 13.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved. | ||
| 520 | |a The present review summarizes the beneficial and detrimental roles of reactive oxygen species in myocardial ischemia/reperfusion injury and cardioprotection. In the first part, the continued need for cardioprotection beyond that by rapid reperfusion of acute myocardial infarction is emphasized. Then, pathomechanisms of myocardial ischemia/reperfusion to the myocardium and the coronary circulation and the different modes of cell death in myocardial infarction are characterized. Different mechanical and pharmacological interventions to protect the ischemic/reperfused myocardium in elective percutaneous coronary interventions and coronary artery bypass grafting, in acute myocardial infarction and in cardiotoxicity from cancer therapy are detailed. The second part keeps the focus on ROS providing a comprehensive overview of molecular and cellular mechanisms involved in ischemia/reperfusion injury. Starting from mitochondria as the main sources and targets of ROS in ischemic/reperfused myocardium, a complex network of cellular and extracellular processes is discussed, including relationships with Ca2+ homeostasis, thiol group redox balance, hydrogen sulfide modulation, cross-talk with NAPDH oxidases, exosomes, cytokines and growth factors. While mechanistic insights are needed to improve our current therapeutic approaches, advancements in knowledge of ROS-mediated processes indicate that detrimental facets of oxidative stress are opposed by ROS requirement for physiological and protective reactions. This inevitable contrast is likely to underlie unsuccessful clinical trials and limits the development of novel cardioprotective interventions simply based upon ROS removal | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Cardioprotection | |
| 650 | 4 | |a Infarct size | |
| 650 | 4 | |a Ischemic conditioning | |
| 650 | 4 | |a Mitochondrion | |
| 650 | 4 | |a Myocardial infarction | |
| 650 | 4 | |a Myocardial ischemia | |
| 650 | 4 | |a Reperfusion | |
| 650 | 7 | |a Reactive Oxygen Species |2 NLM | |
| 700 | 1 | |a Andreadou, Ioanna |e verfasserin |4 aut | |
| 700 | 1 | |a Bell, Robert |e verfasserin |4 aut | |
| 700 | 1 | |a Bertero, Edoardo |e verfasserin |4 aut | |
| 700 | 1 | |a Botker, Hans-Erik |e verfasserin |4 aut | |
| 700 | 1 | |a Davidson, Sean M |e verfasserin |4 aut | |
| 700 | 1 | |a Downey, James |e verfasserin |4 aut | |
| 700 | 1 | |a Eaton, Philip |e verfasserin |4 aut | |
| 700 | 1 | |a Ferdinandy, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Gersh, Bernard J |e verfasserin |4 aut | |
| 700 | 1 | |a Giacca, Mauro |e verfasserin |4 aut | |
| 700 | 1 | |a Hausenloy, Derek J |e verfasserin |4 aut | |
| 700 | 1 | |a Ibanez, Borja |e verfasserin |4 aut | |
| 700 | 1 | |a Krieg, Thomas |e verfasserin |4 aut | |
| 700 | 1 | |a Maack, Christoph |e verfasserin |4 aut | |
| 700 | 1 | |a Schulz, Rainer |e verfasserin |4 aut | |
| 700 | 1 | |a Sellke, Frank |e verfasserin |4 aut | |
| 700 | 1 | |a Shah, Ajay M |e verfasserin |4 aut | |
| 700 | 1 | |a Thiele, Holger |e verfasserin |4 aut | |
| 700 | 1 | |a Yellon, Derek M |e verfasserin |4 aut | |
| 700 | 1 | |a Di Lisa, Fabio |e verfasserin |4 aut | |
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