Defining therapeutic targets for renal fibrosis: Exploiting the biology of pathogenesis - 09/10/21

Doi : 10.1016/j.biopha.2021.112115

Hao Yan ^a, Jiangxin Xu ^a, Zhifei Xu ^a, Bo Yang ^b, Peihua Luo ^a,^⁎ , Qiaojun He ^a,^⁎
^a Center for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China
^b Institute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China

^⁎Correspondence to: Zhejiang University, Zijingang Campus, #866 Yuhangtang Road, Hangzhou, Zhejiang, China.Zhejiang University, Zijingang Campus#866 Yuhangtang RoadHangzhouZhejiangChina

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Abstract

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.

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Graphical Abstract

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Highlights

•	Nearly all resident and infiltrating cells involves in tubulointerstitial fibrosis formation.
•	Phenotypic alterations of almost resident and infiltration cells are discussed.
•	Potential molecules are defined by exploring the mechanism of renal fibrosis.
•	Therapeutic targets and strategies of renal fibrosis are extensively revealed.

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Abbreviations : α-SMA, AKI, CKD, CTGF, DAMPs, ECM, ECs, EndoMT, EMT, IRI, IL, MMPs, NLRP3, NF-κB, TECs, TGF-β, TIMPs, TLRs, UUO