Cell death in heart failure.
Cell death in heart failure.
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DOI：
10.1253/circj.cj-08-0669
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发表时间：
2008-01-01
期刊：
影响因子：
--
通讯作者：
Otsu, Kinya
中科院分区：
文献类型：
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作者：
Nishida, Kazuhiko;Otsu, Kinya
心力衰竭（HF）已成为西方世界和日本的主要心血管疾病，因此迫切需要阐明细胞死亡介导的病理重塑的机制，并找到预防和治疗心力衰竭的方法。历史上，细胞死亡有3种类型：细胞凋亡、自噬和坏死。细胞凋亡是程序性细胞死亡的一种形式，已得到很好的表征，并且细胞凋亡死亡中涉及的分子事件也得到了很好的了解。坏死通常以消极的方式定义：死亡缺乏程序性细胞死亡的特征，因此是意外的和不受控制的。然而，最近的研究表明坏死受到严格调控。自噬是一种细胞生存机制，涉及细胞质成分的降解和回收。与其他两种机制相反，自噬在特定情况下可能介导细胞死亡。事实上，心衰期间已观察到表现出自噬特征的受损心肌细胞。然而，最近的一项研究表明，衰竭心脏中自噬的上调是一种适应性反应。本综述总结了有关心力衰竭心肌细胞死亡分子机制的最新发现。
Heart failure (HF) has become the dominant cardiovascular disorder in the Western world and Japan, so there is an urgent need to clarify the mechanisms governing pathological remodeling mediated through cell death, and to identify ways of preventing and treating HF. Historically, there are 3 types of cell death: apoptosis, autophagy and necrosis. Apoptosis, a form of programmed cell death, has been well characterized and the molecular events involved in apoptotic death are well understood. Necrosis is often defined in a negative manner: death lacking the characteristics of programmed cell death and thus accidental and uncontrolled. However, recent studies indicate that necrosis is tightly regulated. Autophagy is a cell survival mechanism that involves degradation and recycling of cytoplasmic components. In contrast to the other 2 mechanisms, autophagy may mediate cell death under specific circumstances. In fact, damaged cardiomyocytes that show characteristics of autophagy have been observed during HF. However, a recent study indicated that upregulation of autophagy in the failing heart is an adaptive response. This review summarizes recent findings regarding the molecular mechanisms of cardiomyocyte cell death in HF.