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Regulation of cell death in the cardiovascular system.
International Review of Cell and Molecular Biology Pub Date : 2019-12-30 , DOI: 10.1016/bs.ircmb.2019.11.005
Pooja Patel 1 , Jason Karch 2
Affiliation  

The adult heart is a post-mitotic terminally differentiated organ; therefore, beyond development, cardiomyocyte cell death is maladaptive. Heart disease is the leading cause of death in the world and aberrant cardiomyocyte cell death is the underlying problem for most cardiovascular-related diseases and fatalities. In this chapter, we will discuss the different cell death mechanisms that engage during normal cardiac development, aging, and disease states. The most abundant loss of cardiomyocytes occurs during a myocardial infarction, when the blood supply to the heart is obstructed, and the affected myocardium succumbs to cell death. Originally, this form of cell death was considered to be unregulated; however, research from the last half a century clearly demonstrates that this form of cell death is multifaceted and employees various degrees of regulation. We will explore all of the cell death pathways that have been implicated in this disease state and the potential interplay between them. Beyond myocardial infarction, we also explore the role and mechanisms of cardiomyocyte cell death in heart failure, myocarditis, and chemotherapeutic-induced cardiotoxicity. Inhibition of cardiomyocyte cell death has extensive therapeutic potential that will increase the longevity and health of the human heart.

中文翻译:

调节心血管系统中细胞的死亡。

成年心脏是有丝分裂后的终末分化器官。因此,除了发展之外,心肌细胞死亡是适应不良的。心脏病是世界上主要的死亡原因,而心肌细胞异常死亡是大多数与心血管有关的疾病和死亡的根本问题。在本章中,我们将讨论在正常心脏发育,衰老和疾病状态下参与的不同细胞死亡机制。心肌细胞的损失最多,发生在心肌梗塞期间,此时心脏的血液供应受阻,受影响的心肌屈服于细胞死亡。最初,这种形式的细胞死亡被认为是不受监管的;然而,近半个世纪的研究清楚地表明,这种细胞死亡形式是多方面的,并且员工有不同程度的调节。我们将探索与该疾病状态有关的所有细胞死亡途径,以及它们之间的潜在相互作用。除心肌梗塞外,我们还探讨了心肌细胞死亡在心力衰竭,心肌炎和化疗引起的心脏毒性中的作用和机制。抑制心肌细胞死亡具有广泛的治疗潜力,将增加人类心脏的寿命和健康。我们还探讨了心肌细胞死亡在心力衰竭,心肌炎和化疗引起的心脏毒性中的作用和机制。抑制心肌细胞死亡具有广泛的治疗潜力,将增加人类心脏的寿命和健康。我们还探讨了心肌细胞死亡在心力衰竭,心肌炎和化疗引起的心脏毒性中的作用和机制。抑制心肌细胞死亡具有广泛的治疗潜力,将增加人类心脏的寿命和健康。
更新日期:2019-12-30
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