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Autophagy: molecular machinery regulation and implications for renalpathophysiology

机译:自噬:分子机制调控及其对肾脏的影响病理生理学

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摘要

Autophagy is a cellular process of “self-eating.” During autophagy, a portion of cytoplasm is enveloped in double membrane-bound structures called autophagosomes, which undergo maturation and fusion with lysosomes for degradation. At the core of the molecular machinery of autophagy is a specific family of genes or proteins called Atg. Originally identified in yeast, Atg orthologs are now being discovered in mammalian cells and have been shown to play critical roles in autophagy. Traditionally, autophagy is recognized as a cellular response to nutrient deprivation or starvation whereby cells digest cytoplasmic organelles and macromolecules to recycle nutrients for self-support. However, studies during the last few years have indicated that autophagy is a general cellular response to stress. Interestingly, depending on experimental conditions, especially stress levels, autophagy can directly induce cell death or act as a mechanism of cell survival. In this review, we discuss the molecular machinery, regulation, and function of autophagy. In addition, we analyze the recent findings of autophagy in renal systems and its possible role in renal pathophysiology.
机译:自噬是细胞“自我饮食”的过程。在自噬过程中,一部分细胞质被称为自噬体的双膜结合结构包裹,该结构经历成熟并与溶酶体融合降解。自噬分子机制的核心是称为Atg的特定基因或蛋白质家族。 Atg直系同源物最初在酵母中鉴定,现已在哺乳动物细胞中发现,并已显示在自噬中起关键作用。传统上,自噬被认为是对营养缺乏或饥饿的细胞反应,从而使细胞消化细胞质细胞器和大分子以回收营养以自我支持。然而,最近几年的研究表明自噬是细胞对压力的一般反应。有趣的是,取决于实验条件,尤其是应激水平,自噬可以直接诱导细胞死亡或充当细胞存活的机制。在这篇综述中,我们讨论了自噬的分子机制,调控和功能。此外,我们分析了自噬在肾脏系统中的最新发现及其在肾脏病理生理中的可能作用。

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