Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease.
Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease.
复制标题
细胞衰老影响缺血性心脏病的心脏再生和修复
DOI：
10.14336/ad.2020.0811
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发表时间：
2021-04
影响因子：
7.4
通讯作者：
Huang W
中科院分区：
文献类型：
--
作者：
Yan C;Xu Z;Huang W
缺血性心脏病（IHD）是缺血性心肌病的一种综合征。缺血心肌中的肌生成和血管生成对于IHD后的心肌细胞（CM）存活、改善心功能和减缓心力衰竭的进展是重要的。细胞衰老是由应激引起的永久性不可逆细胞周期停滞的状态，其导致细胞功能下降，例如增殖、迁移、归巢和分化。此外，衰老细胞产生衰老相关分泌表型（SASP），其通过分泌促炎细胞因子、趋化因子、生长因子和细胞外基质降解蛋白来影响组织微环境和周围细胞。心血管相关衰老细胞（包括血管内皮细胞（VECs）、血管平滑肌细胞（VSMCs）、CM和祖细胞）的积累是心血管疾病（如血管老化、动脉粥样硬化斑块形成、心肌梗死（MI）和心室重构）的重要危险因素。本文就缺血性心脏病后血管生成、肌生成和细胞衰老的研究进展作一综述。此外，本文还对细胞衰老与心血管疾病的关系以及细胞衰老的机制进行了综述。最后，我们讨论了一个潜在的治疗策略MI靶向衰老细胞。
Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.