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Defining therapeutic targets for renal fibrosis: Exploiting the biology of pathogenesis
Hao Yan1, Jiangxin Xu1, Zhifei Xu1
1Center for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
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.
Insights
Renal fibrosis, a hallmark of chronic kidney disease (CKD), involves excessive matrix deposition. This review explores cellular mechanisms and highlights new therapeutic targets for kidney fibrosis.
Area of Science:
- Nephrology
- Pathology
- Cell Biology
Background:
- Renal fibrosis is a common endpoint for chronic kidney diseases (CKDs), characterized by failed wound healing.
- It involves fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to kidney damage and dysfunction.
- Current treatments lack specific efficacy against renal fibrosis itself.
Purpose of the Study:
- To review recent advancements in understanding cellular participation and interactions in renal fibrosis.
- To comprehensively discuss the mechanisms of renal fibrosis at the cellular level.
- To identify novel therapeutic targets and approaches for treating renal fibrosis.
Main Methods:
- Literature review of recent research on renal fibrosis.
- Analysis of cellular and molecular mechanisms driving fibrosis.
- Synthesis of information on cell types involved in kidney fibrosis.
Main Results:
- Detailed summary of resident and infiltrated cell roles in renal fibrosis.
- Comprehensive discussion of the cellular mechanisms underlying fibrosis progression.
- Identification of key cellular players and their interactions in kidney fibrosis.
Conclusions:
- Renal fibrosis is a complex cellular process involving multiple cell types.
- Understanding these cellular interactions is crucial for developing targeted therapies.
- Novel therapeutic strategies targeting specific cellular mechanisms show promise for treating renal fibrosis.
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