Cardiomyocyte autophagy: remodeling, repairing, and reconstructing the heart.
Cardiomyocyte autophagy: remodeling, repairing, and reconstructing the heart.
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DOI：
10.1007/s11906-009-0070-1
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发表时间：
2009-12
影响因子：
5.6
通讯作者：
Hill, Joseph A.
中科院分区：
文献类型：
--
作者：
Cao, Dian J.;Gillette, Thomas G.;Hill, Joseph A.
自噬是一种进化上保守的分解代谢途径，它依赖于溶酶体而导致受损蛋白质和细胞器的周转。当营养素供应不足时，通过自噬大量去除细胞质成分可以补充耗尽的能量储存，这是维持细胞动态平衡的关键过程。然而，自噬途径的长期激活可能会导致细胞死亡。长期的证据表明，溶酶体途径的刺激与病理性心脏重塑和包括心力衰竭和缺血在内的许多心脏疾病有关。然而，直到最近，才开始从有助于疾病发病机制的自噬中解析出细胞保护性自噬。目前的想法表明，自噬的影响存在于一个连续体上，触发因素、自噬通量的持续时间和幅度，以及可能的目标细胞内货物是最终结果的关键决定因素。破译自噬如何参与心脏的基础内稳态、衰老和疾病发病机制，可能会发现在心脏病治疗中具有临床相关性的新见解。
Autophagy is an evolutionarily conserved catabolic pathway of lysosome-dependent turnover of damaged proteins and organelles. When nutrients are in short supply, bulk removal of cytoplasmic components by autophagy replenishes depleted energy stores, a process critical for maintaining cellular homeostasis. However, prolonged activation of autophagic pathways can result in cell death. Longstanding evidence has linked the stimulation of lysosomal pathways to pathologic cardiac remodeling and a number of cardiac diseases, including heart failure and ischemia. Only recently, however, has work begun to parse cyto-protective autophagy from autophagy that contributes to disease pathogenesis. Current thinking suggests that the effects of autophagy exist on a continuum, with the eliciting triggers, the duration and amplitude of autophagic flux, and possibly the targeted intra cellular cargo as critical determinants of the end result. Deciphering how autophagy participates in basal homeostasis of the heart, in aging, and in disease pathogenesis may uncover novel insights with clinical relevance in the treatment of heart disease.
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影响因子：
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