自噬及其在肾纤维化中的作用研究进展

Advances in autophagy and its role in renal fibrosis

自噬是细胞在应激条件下通过溶酶体途径对自身组分进行分解代谢和循环利用的过程,是细胞的一种适应性反应和保护机制,并且与许多生物学过程和疾病密切相关。在进行性肾脏疾病中,肾纤维化是终末期肾衰竭的共同途径。最近研究表明,转化生长因子β1(TGF-β1)作为一种多效细胞因子和肾纤维化的中枢介质可调节自噬,而自噬可调节肾纤维化的许多关键途径,如肾小管间质纤维化。深入认识自噬的分子机制和信号通路,及其在进行性肾纤维化中的作用,可能为肾纤维化找到潜在的有效治疗靶点。

Autophagy is a process in which cells catabolize and recycle their components through lysosomal pathways under stress conditions. It is an adaptive response and protective mechanism of cells and is closely related to many biological processes and diseases. In progressive kidney disease, renal fibrosis is a common pathway for end-stage renal failure. Recent studies have shown that transforming growth factor β1(TGF-β1) acts as a central mediator of pleiotropic cytokines and renal fibrosis, and autophagy regulates many key pathways of renal fibrosis, such as tubulointerstitial fibers. Chemical. An in-depth understanding of the molecular mechanisms and signaling pathways of autophagy and their role in progressive renal fibrosis may find potential effective therapeutic targets for renal fibrosis.