Activation of autophagy contributes to the renoprotective effect of postconditioning on acute kidney injury and renal fibrosis
Activation of autophagy contributes to the renoprotective effect of postconditioning on acute kidney injury and renal fibrosis
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DOI：
10.1016/j.bbrc.2018.09.003
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发表时间：
2018-10-12
影响因子：
3.1
通讯作者：
Tan, Xiaohua
中科院分区：
文献类型：
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作者：
Song, Yaolin;Tao, Qianyu;Tan, Xiaohua
缺血/再灌注损伤导致急性肾损伤（阿基）和随后的慢性肾病（CKD），包括肾纤维化。自噬是一种细胞质成分降解途径，在肾脏纤维化等多种疾病的发生发展中起着复杂的作用。我们的前期工作表明，后处理（POC）通过抑制再灌注后活性氧（ROS）的过度产生，对肾纤维化具有良好的治疗作用。但自噬和POC在肾保护作用中的联系尚不清楚。在这里，我们定义了自噬和POC在对阿基和随后的肾纤维化的保护作用中的相关性。我们发现，在I/R损伤后两天，POC大大减少肾小管上皮细胞凋亡和改善肾功能;自噬在POC大鼠肾脏中显著激活。再灌注后2个月，I/R损伤大鼠表现出严重的肾纤维化和上皮间质转化（EMT），而POC治疗组大鼠的这些明显减弱。总之，我们的研究结果证明，POC可以通过增强自噬激活来减轻I/R损伤后的肾损害并减轻EMT的程度。(C)2018由Elsevier Inc.出版
Ischemia/Reperfusion injury contributes to acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) including renal fibrosis. Autophagy is a cytoplasmic components degradation pathway that has complex function in the development of various diseases such as fibrosis in kidney. Our previous work demonstrated that postconditioning (POC) showed excellent therapeutic effect on renal fibrosis via inhibiting the overproduction of reactive oxygen species (ROS) after reperfusion. But the connection of autophagy and POC in the renoprotective effect remains unclear. Here, we defined the relevance of autophagy and POC in the protective effect on AKI and subsequent renal fibrosis. We found that at two days after I/R injury, POC largely reduced renal tubular epithelial cell apoptosis and improved renal function; autophagy was significantly activated in kidneys of the POC rats. At two months after reperfusion, the I/R injury rats displayed severe renal fibrosis and epithelial-mesenchymal transition (EMT), whereas these were remarkably attenuated in the POC treated rats. Overall, our results derrionstrated that POC could reduce renal damage and attenuate the degree of EMT after I/R injury via enhanced activation of autophagy. (C) 2018 Published by Elsevier Inc.