Autophagy in acute kidney injury.
Autophagy in acute kidney injury.
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DOI：
10.1016/j.semnephrol.2013.11.004
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发表时间：
2014-01
影响因子：
3.3
通讯作者：
Dong, Zheng
中科院分区：
文献类型：
--
作者：
Livingston, Man J.;Dong, Zheng
急性肾损伤是一种与不良临床结果相关的主要肾脏疾病。急性肾损伤的发病机制是多因素的，其特点是肾小管细胞损伤和死亡。最近的研究表明，急性肾损伤期间近端肾小管细胞会诱导自噬。人们对肾小管细胞自噬的调控机制知之甚少；然而，最近的一些发现为进一步调查奠定了基础。尽管自噬在某些实验条件下可能促进细胞死亡，但药理学和自噬相关基因敲除研究已经确立了自噬在急性肾损伤中的肾脏保护作用。讨论了自噬保护细胞免受损伤的机制，以及在某些条件下其促生存作用如何可能转变为促死亡作用。进一步的研究有望帮助我们了解肾小管细胞自噬的调控网络，明确其在急性肾损伤特定背景下的精确作用，并确定预防和治疗急性肾损伤的自噬靶向策略。
Acute kidney injury is a major kidney disease associated with poor clinical outcomes. The pathogenesis of acute kidney injury is multifactorial and is characterized by tubular cell injury and death. Recent studies have demonstrated autophagy induction in proximal tubular cells during acute kidney injury. The regulatory mechanisms of tubular cell autophagy are poorly understood; however, some recent findings have set up a foundation for further investigation. Although autophagy may promote cell death under certain experimental conditions, pharmacological and autophagy-related gene knockout studies have established a renoprotective role for autophagy in acute kidney injury. The mechanisms by which autophagy protects cells from injury and how, possibly, its pro-survival role switches to pro-death under certain conditions are discussed. Further research is expected to help us understand the regulatory network of tubular cell autophagy, define its precise roles in specific context of acute kidney injury, and identify autophagy-targeting strategies for the prevention and treatment of acute kidney injury.
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发表时间：
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影响因子：
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