Yan Hao, Xu Jiangxin, Xu Zhifei, Yang Bo, Luo Peihua, He Qiaojun
Center for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Institute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Biomed Pharmacother. 2021 Nov;143:112115. doi: 10.1016/j.biopha.2021.112115. Epub 2021 Sep 3.
Renal fibrosis is a failed wound-healing process of the kidney tissue after chronic, sustained injury, which is a common pathway and pathological marker of virtually every type of chronic kidney disease (CKD), regardless of cause. However, there is a lack of effective treatment specifically targeting against renal fibrosis per se to date. The main pathological feature of renal fibrosis is the massive activation and proliferation of renal fibroblasts and the excessive synthesis and secretion of extracellular matrix (ECM) deposited in the renal interstitium, leading to structural damage, impairment of renal function, and eventually end-stage renal disease. In this review, we summarize recent advancements regarding the participation and interaction of many types of kidney residents and infiltrated cells during renal fibrosis, attempt to comprehensively discuss the mechanism of renal fibrosis from the cellular level and conclude by highlighting novel therapeutic targets and approaches for development of new treatments for patients with renal fibrosis.
肾纤维化是肾脏组织在慢性持续性损伤后愈合过程失败的结果,它是几乎每种类型慢性肾脏病(CKD)的共同途径和病理标志,无论病因如何。然而,迄今为止,缺乏专门针对肾纤维化本身的有效治疗方法。肾纤维化的主要病理特征是肾成纤维细胞大量活化和增殖,以及肾间质中细胞外基质(ECM)过度合成和分泌,导致结构损伤、肾功能损害,最终发展为终末期肾病。在本综述中,我们总结了肾纤维化过程中多种肾脏固有细胞和浸润细胞的参与及相互作用的最新进展,试图从细胞水平全面探讨肾纤维化的机制,并通过强调新的治疗靶点和开发肾纤维化患者新治疗方法的途径来进行总结。