Novel Insights into Molecular Mechanisms of Renal Fibrosis

Dear Colleagues,

A hallmark of chronic kidney disease is renal fibrosis, which is characterized by excessive production and deposition of extracellular matrix leading to disruption of renal parenchyma and progressive loss of kidney function to end-stage kidney disease. Fibrogenesis of the kidney is a complex process resulting from tubular epithelial cell damage, infiltration and activation of bone marrow-derived cells such as macrophages, T cells, and fibroblast precursors, and activation of interstitial fibroblasts. Activated fibroblasts/myofibroblasts produce excessive amounts of extracellular matrix, which impairs normal kidney structure and causes progressive loss of kidney function. Currently, there is no effective treatment for renal fibrosis. Therefore, there is an urgent need to understand the molecular and cellular mechanisms underlying the pathogenesis of renal fibrosis and develop novel therapeutic strategies. Matrix-producing fibroblasts/myofibroblasts are the major sources of extracellular matrix. Recent studies indicate that these cells may derive from multiple sources including resident fibroblasts, tubular epithelial cells/endothelial cells, and bone marrow precursors/fibrocytes. A number of chemokines, cytokines, and signaling pathways have been reported to play a role in the development of renal fibrosis including MCP-1, CXCL16, transforming growth factor-β (TGF-β)/Smad, platelet-derived growth factors (PDGF), adiponectin, IL-4, IL-13, JAK/STAT, AMP-activated protein kinase (AMPK), Wnt/β-catenin, notch signaling, hedgehog signaling, integrins, renin-angiotensin-aldosterone system, and endothelin. Recently, omics-based approaches have provided additional insights into the molecular mechanisms and therapeutic targets of renal fibrosis.

In this research topic, we welcome submission of original research articles, perspectives, and reviews on current understanding of the cellular and molecular mechanisms of renal fibrosis as well as development of novel therapeutic strategies for renal fibrosis.

Prof. Dr. Yanlin Wang
Guest Editor

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• renal fibrosis
• chronic kidney disease
• fibroblasts
• extracellualr matrix
• inflammation
• cell signaling