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©2013 Baishideng Publishing Group Co., Limited. All rights reserved.
Matrix metalloproteinases contribute to kidney fibrosis in chronic kidney diseases
Hong Zhao, Yanting Dong, Department of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan 030001, Shaanxi Province, China
Xinrui Tian, Zhuola Liu, Department of Respiratory Medicine, the Second Hospital of Shanxi Medical University, Taiyuan 030001, Shaanxi Province, China
Yun Zhang, Experimental Centre of Science and Research, the First Clinical Hospital of Shanxi Medical University, Taiyuan 030001, Shaanxi Province, China
Thian Kui Tan, Ye Zhao, David CH Harris, Guoping Zheng, Centre for Transplantation and Renal Research, Westmead Millennium Institute, the University of Sydney, NSW 2145, Sydney, Australia
Author contributions: ALL authors contributed to this manuscript in writing, study results and approval of the manuscript.
Correspondence to: Guoping Zheng, MD, PhD, Centre for Transplantation and Renal Research, Westmead Millennium Institute, the University of Sydney, City Road, NSW 2145, Sydney, Australia. guoping.zheng@sydney.edu.au
Telephone: +61-2-98459582 Fax: +61-2-98459620
Received: June 29, 2013
Revised: August 1, 2013
Accepted: August 3, 2013
Published online: August 6, 2013
Revised: August 1, 2013
Accepted: August 3, 2013
Published online: August 6, 2013
Core Tip
Core tip: Matrix metalloproteinases (MMPs) were previously known to be anti-fibrotic for their ability to degrade and remodel extracellular matrix proteins. Recent studies including our own have shown that MMPs are implicated in initiation and progression of kidney fibrosis. MMP-9 of both tubular and macrophage origins were found to be able to induce epithelial-mesenchymal transition of tubular cells, an important mechanism causing kidney fibrosis. This review, by focus on MMP-9 and epithelial–mesenchymal transition, seeks to provide a comprehensive understanding for the roles of MMPs in kidney fibrosis.