Hypoxia-inducible factor-1 : Regulatory mechanisms and drug therapy in myocardial infarction
Copyright © 2023 Elsevier B.V. All rights reserved..
Myocardial infarction (MI), an acute cardiovascular disease characterized by coronary artery blockage, inadequate blood supply, and subsequent ischemic necrosis of the myocardium, is one of the leading causes of death. The cellular, physiological, and pathological responses following MI are complex, involving multiple intertwined pathological mechanisms. Hypoxia-inducible factor-1 (HIF-1), a crucial regulator of hypoxia, plays a significant role in of the development of MI by modulating the behavior of various cells such as cardiomyocytes, endothelial cells, macrophages, and fibroblasts under hypoxic conditions. HIF-1 regulates various post-MI adaptive reactions to acute ischemia and hypoxia through various mechanisms. These mechanisms include angiogenesis, energy metabolism, oxidative stress, inflammatory response, and ventricular remodeling. With its crucial role in MI, HIF-1 is expected to significantly influence the treatment of MI. However, the drugs available for the treatment of MI targeting HIF-1 are currently limited, and most contain natural compounds. The development of precision-targeted drugs modulating HIF-1 has therapeutic potential for advancing MI treatment research and development. This study aimed to summarize the regulatory role of HIF-1 in the pathological responses of various cells following MI, the diverse mechanisms of action of HIF-1 in MI, and the potential drugs targeting HIF-1 for treating MI, thus providing the theoretical foundations for potential clinical therapeutic targets.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:963 |
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| Enthalten in: |
European journal of pharmacology - 963(2024) vom: 15. Jan., Seite 176277 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Pan, Jinyuan [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 08.01.2024 Date Revised 27.01.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.ejphar.2023.176277 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Myocardial infarction (MI), an acute cardiovascular disease characterized by coronary artery blockage, inadequate blood supply, and subsequent ischemic necrosis of the myocardium, is one of the leading causes of death. The cellular, physiological, and pathological responses following MI are complex, involving multiple intertwined pathological mechanisms. Hypoxia-inducible factor-1 (HIF-1), a crucial regulator of hypoxia, plays a significant role in of the development of MI by modulating the behavior of various cells such as cardiomyocytes, endothelial cells, macrophages, and fibroblasts under hypoxic conditions. HIF-1 regulates various post-MI adaptive reactions to acute ischemia and hypoxia through various mechanisms. These mechanisms include angiogenesis, energy metabolism, oxidative stress, inflammatory response, and ventricular remodeling. With its crucial role in MI, HIF-1 is expected to significantly influence the treatment of MI. However, the drugs available for the treatment of MI targeting HIF-1 are currently limited, and most contain natural compounds. The development of precision-targeted drugs modulating HIF-1 has therapeutic potential for advancing MI treatment research and development. This study aimed to summarize the regulatory role of HIF-1 in the pathological responses of various cells following MI, the diverse mechanisms of action of HIF-1 in MI, and the potential drugs targeting HIF-1 for treating MI, thus providing the theoretical foundations for potential clinical therapeutic targets | ||
| 650 | 4 | |a Journal Article | |
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| 650 | 4 | |a Hypoxia | |
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| 650 | 4 | |a Oxidative stress | |
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| 700 | 1 | |a Li, Dongxiao |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Yuan |e verfasserin |4 aut | |
| 700 | 1 | |a Lu, Mengkai |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Yuanlong |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, Bowen |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Zhiyuan |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Chao |e verfasserin |4 aut | |
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