自噬与急性肾损伤

Autophagy and acute kidney injury

自噬对于维持肾脏细胞存活及细胞稳态至关重要，并参与多种肾脏疾病的发生发展。急性肾损伤能激活肾脏细胞自噬；但其具体调控机制目前仍不明确，可能与氧化应激、内质网应激、缺氧诱导因子-1α、抑癌基因p53和Bcl-2家族等有关。自噬在急性肾损伤的病理生理过程中的作用尚存在争议，多认为自噬具有重要的保护作用。自噬将成为预防和治疗急性肾损伤潜在的新靶点。

Not only does autophagy play a vital role in maintaining kidney cell survival and homeostasis,but al-so it is involved in the pathophysiology of several kidney diseases. Recent studies have indicated that autophagy was ac-tivated in kidney cells during acute kidney injury and its regulatory mechanism was unclear. Autophagy activation in kidney may be associated with oxidative stress, endoplasmic reticulum stress, hypoxia inducible factor-1α, p53 and Bcl-2 family. The role of autophagy in acute kidney injury is still controversial. Most believe that it plays a protective role during acute kidney injury. Therefore autophagy will become a novel and potential target for the prevention and treatment of acute kidney injury.