Programmed cardiomyocyte death in myocardial infarction.

IF 6.1 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Hao Wu, Qi Lan, Yi-Xiang He, Jin-Yi Xue, Hao Liu, Yuan Zou, Ping Liu, Gang Luo, Ming-Tai Chen, Meng-Nan Liu
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引用次数: 0

Abstract

Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI. By gaining a deeper understanding of the mechanisms of cardiomyocyte death, it aims to provide new insights into the prevention and treatment of MI.

心肌梗死中的程序性心肌细胞死亡。
心血管疾病(CVD)是世界范围内人类死亡的主要原因,患者通常在心肌梗死(MI)中存在心力衰竭(HF)的高风险,心肌梗死(MI)是一种常见的CVD形式,由于心肌灌注不足导致心肌细胞死亡和心肌坏死。作为终末分化的细胞,心肌细胞的再生能力严重受限,过量死亡的心肌细胞会进一步对存活细胞造成压力,有可能加剧更广泛的心脏病。本文重点探讨心肌细胞程序性死亡(PCD)(包括不同形式的凋亡、坏死和自噬)与心肌梗死之间的关系,以及这些机制在心肌梗死治疗中的潜在应用。通过对心肌细胞死亡机制的深入了解,旨在为心肌梗死的预防和治疗提供新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Apoptosis
Apoptosis 生物-生化与分子生物学
CiteScore
9.10
自引率
4.20%
发文量
85
审稿时长
1 months
期刊介绍: Apoptosis, a monthly international peer-reviewed journal, focuses on the rapid publication of innovative investigations into programmed cell death. The journal aims to stimulate research on the mechanisms and role of apoptosis in various human diseases, such as cancer, autoimmune disease, viral infection, AIDS, cardiovascular disease, neurodegenerative disorders, osteoporosis, and aging. The Editor-In-Chief acknowledges the importance of advancing clinical therapies for apoptosis-related diseases. Apoptosis considers Original Articles, Reviews, Short Communications, Letters to the Editor, and Book Reviews for publication.
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