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细胞自噬及其在肾缺血再灌注损伤中潜在调节因子的研究进展。

Advances on Cell Autophagy and Its Potential Regulatory Factors in Renal Ischemia-Reperfusion Injury.

机构信息

Faculty of Chinese Medicine, Macau University of Science and Technology, Taipa, People's Republic of China.

State Key Laboratory of Quality Research in Chinese Medicines (Macau University of Science and Technology), Taipa, People's Republic of China.

出版信息

DNA Cell Biol. 2019 Sep;38(9):895-904. doi: 10.1089/dna.2019.4767. Epub 2019 Jul 26.

Abstract

Ischemia-reperfusion injury is a major reason for acute kidney injury and various kidney diseases. Autophagy plays an important role during renal ischemia-reperfusion injury (RIRI), but it remains controversial whether autophagy contributes to cell survival or ischemia-reperfusion-induced cell death. In the review, we summarized the function of autophagy in the progression of acute ischemic kidney injury, as well as its related molecular mechanisms. While analyzing the opposite roles of autophagy in RIRI, it was concluded that the protective or detrimental function of autophagy was depending on the timing and amount of the activation of cell autophagy. We also summarized the regulatory agents, including active compounds, proteins, or microRNAs (miRNAs), which regulated the cell autophagy during renal acute ischemic kidney injury process. This explained why the opposite conclusion occurred when cell autophagy was studied in the RIRI models from different researchers. Therefore, the article provided a hypothesis to control cell autophagy at the appropriate timing and intensity so as to alleviate renal injury and sustain cell survival of the renal cell.

摘要

缺血再灌注损伤是急性肾损伤和各种肾脏疾病的主要原因。自噬在肾缺血再灌注损伤(RIRI)中起着重要作用,但自噬是否有助于细胞存活或缺血再灌注诱导的细胞死亡仍存在争议。在综述中,我们总结了自噬在急性缺血性肾损伤进展中的作用及其相关的分子机制。在分析自噬在 RIRI 中的相反作用时,得出结论认为自噬的保护或有害功能取决于细胞自噬激活的时间和数量。我们还总结了调节自噬的调节剂,包括活性化合物、蛋白质或 microRNAs(miRNAs),它们在肾急性缺血性肾损伤过程中调节细胞自噬。这解释了为什么在不同研究人员的 RIRI 模型中研究细胞自噬时会得出相反的结论。因此,本文提供了一个假设,即在适当的时间和强度控制细胞自噬,以减轻肾损伤并维持肾细胞的存活。

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