Cell death in the myocardium: my heart won't go on.

Cell death in the myocardium: my heart won't go on.
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DOI:
10.1002/iub.1180
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发表时间:
2013-08
期刊:
影响因子:
4.6
通讯作者:
Gustafsson, Asa B.
Gustafsson, Asa B.
中科院分区:
生物学3区
文献类型:
--
作者:
Orogo, Amabel M.;Gustafsson, Asa B.

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心肌细胞的丢失在心力衰竭的发病机制中起着关键作用。由于心肌细胞减少,心脏无法维持有效的收缩。心肌细胞死亡机制的研究一直是人们关注的焦点,其最终目的是减少心肌细胞的损伤程度,改善衰竭心肌的功能。心肌细胞的坏死和凋亡都会导致心肌细胞的丢失,而这种细胞的丢失是心脏病理的一个标志,包括缺血/再灌注、心肌梗死和心力衰竭。细胞凋亡是一个高度调控的过程,通过质膜上的死亡受体或通过线粒体的通透性来激活。坏死通常被认为是一个不受控制的过程,导致线粒体肿胀、细胞破裂和随后的炎症。然而,最近的研究发现了一条介导调节性坏死或坏死性下垂的信号通路。线粒体在细胞的凋亡和坏死中都起着重要的作用,线粒体的形态变化会影响细胞对应激的敏感性。本文重点介绍了心肌细胞死亡的各种方式,并着重介绍了它们是如何在应激反应中导致心肌细胞丢失的。
Loss of cardiomyocytes plays a critical role in the pathogenesis of heart failure. With fewer myocytes, the heart is unable to sustain efficient contraction. Much attention has been focused on understanding mechanisms of cell death in myocytes with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Both necrosis and apoptosis contribute to loss of myocytes, and this loss of cells is a hallmark of cardiac pathologies, including ischemia/reperfusion, myocardial infarction, and heart failure. Apoptosis is a highly regulated process that is activated via death receptors in the plasma membrane or via permeabilization of the mitochondria. Necrosis is generally viewed as an uncontrolled process that leads to mitochondrial swelling, cell rupture, and subsequent inflammation. However, recent studies have uncovered a signaling pathway that mediate regulated necrosis, or necroptosis. Mitochondria play an important role in both apoptosis and necrosis, and changes in their morphology can affect the cells’ susceptibility to stress. This review focuses on the various modes of cell death in the myocardium and highlights how they contribute to loss of myocytes in response to stress.
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