Matrix metalloproteinases contribute to kidney fibrosis in chronic kidney diseases

Hong Zhao1, Yanting Dong, Xinrui Tian

  • 1Hong Zhao, Yanting Dong, Department of Biochemistry and Molecular Biology, Shanxi Medical University, Taiyuan 030001, Shaanxi Province, China.

World Journal of Nephrology
|November 21, 2013
PubMed

Insights

Matrix metalloproteinases (MMPs), particularly MMP-9, promote kidney fibrosis by inducing epithelial-mesenchymal transition (EMT). Targeting MMP-9 offers a potential therapeutic strategy for chronic kidney disease.

Area of Science:

  • Nephrology
  • Cell Biology
  • Biochemistry

Background:

  • Matrix metalloproteinases (MMPs) were initially considered anti-fibrotic due to their extracellular matrix remodeling capabilities.
  • Emerging evidence implicates MMPs in kidney fibrosis progression via epithelial-mesenchymal transition (EMT), endothelial-mesenchymal transition (EndoMT), and fibroblast activation.

Purpose of the Study:

  • To comprehensively review the role of MMPs, with a specific focus on MMP-9, in the pathogenesis of kidney fibrosis.
  • To highlight the contribution of MMP-9 to tubular cell EMT and its implications for chronic kidney disease.

Main Methods:

  • Review of existing literature on MMPs, kidney fibrosis, and EMT.
  • Analysis of studies investigating MMP-9 expression and function in kidney disease models.
  • Focus on the interplay between transforming growth factor-β (TGF-β) and MMP-9 in inducing EMT.

Main Results:

  • MMPs, especially MMP-9 secreted by macrophages, are now recognized as profibrotic factors.
  • MMP-9 induces tubular cell EMT, a key driver of kidney fibrosis.
  • Transforming growth factor-β1 (TGF-β1) up-regulates MMP-9 in kidney tubular epithelial cells and activates macrophages.

Conclusions:

  • MMP-9 plays a significant profibrotic role in kidney disease by promoting EMT.
  • Targeting MMP-9 presents a promising therapeutic avenue for preventing or treating kidney fibrosis in chronic kidney disease.

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