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Published on: September 3, 2020
Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease
Chi Yan1,2,3, Zhimeng Xu4, Weiqiang Huang1,2,3
11Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi, China.
Insights
Cellular senescence, a state of irreversible cell cycle arrest, contributes to ischemic heart disease (IHD) progression. Targeting senescent cells offers a potential therapeutic strategy for myocardial infarction (MI).
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Regenerative Medicine
Background:
- Ischemic heart disease (IHD) involves cardiomyocyte (CM) damage, where myogenesis and angiogenesis are crucial for recovery.
- Cellular senescence, a stress-induced permanent cell cycle arrest, impairs cellular functions and promotes inflammation via the senescence-associated secretory phenotype (SASP).
- Accumulation of senescent cells (vascular endothelial cells, vascular smooth muscle cells, CMs, progenitor cells) is linked to cardiovascular diseases like myocardial infarction (MI) and ventricular remodeling.
Purpose of the Study:
- To review the processes of angiogenesis, myogenesis, and cellular senescence following IHD.
- To elucidate the relationship between cellular senescence and cardiovascular disease.
- To discuss potential therapeutic strategies targeting senescent cells for MI.
Main Methods:
- Literature review summarizing current research on IHD, cellular senescence, and cardiovascular disease.
- Analysis of the mechanisms underlying cellular senescence in the context of IHD.
- Exploration of therapeutic approaches targeting senescent cells.
Main Results:
- Cellular senescence impairs essential cardiac repair mechanisms like myogenesis and angiogenesis after IHD.
- Senescent cells and their SASP contribute to the progression of cardiovascular diseases, including MI and adverse ventricular remodeling.
- Targeting senescent cells presents a promising therapeutic avenue for managing IHD and MI.
Conclusions:
- Cellular senescence plays a significant role in the pathophysiology of IHD and its complications.
- Understanding the mechanisms of senescence in the heart is critical for developing effective treatments.
- Therapeutic strategies aimed at senescent cells hold potential for improving outcomes in patients with ischemic heart disease.
Abstract:
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.
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