基于巨噬细胞-肌成纤维细胞转分化的肾间质纤维化病理机制及药物干预作用

Pathological Mechanism and Drug Intervention of Renal Interstitial Fibrosis Based on Macrophage-Myofibroblast Transdifferentiation

在肾间质纤维化过程中,骨髓中募集的巨噬细胞可在损伤的肾脏中直接转化为肌成纤维细胞。巨噬细胞-肌成纤维细胞转分化(MMT)是肾间质纤维化的重要病理机制之一。在MMT过程中,巨噬细胞的活化受转化生长因子-β1、Janus激酶3/信号转导及转录活化因子6、Wnt等信号通路调控,阻断这些信号通路可抑制MMT,改善肾间质纤维化。在临床及体内外实验中,针对防治肾纤维化的药物干预研究较活跃,其中某些药物的干预作用可能与巨噬细胞及MMT相关。因此,深入研究肾脏MMT的病理机制及药物干预作用可以为相关疾病的治疗提供新思路。

In the process of renal fibrosis,macrophages recruited from bone marrow can be directly converted into myofibroblasts in the injured kidney.Macrophage-myofibroblast transdifferentiation(MMT)is one of the important pathological mechanisms of renal interstitial fibrosis.During MMT,macrophage activation is regulated by signal pathways of transforming growth factor-β1,Janus kinase 3/signal transducer and activator of transcription 6,Wnt etc.Blocking these signal pathways can inhibit MMT and improve renal interstitial fibrosis.In clinical and in vitro experiments,drug intervention for prevention and treatment of renal fibrosis is more active,and the intervention effect of some drugs may be related to macrophages and MMT.Therefore,the in-depth study of the pathological mechanism of renal MMT and the intervention effect of drugs can provide new ideas for the treatment of related diseases.