Related Experiment Video
Updated: May 5, 2026

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
Published on: April 25, 2025
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.
Abstract:
Matrix metalloproteinases (MMPs) are members of the neutral proteinase family. They were previously thought to be anti-fibrotic because of their ability to degrade and remodel of extracellular matrix. However, recent studies have shown that MMPs are implicated in initiation and progression of kidney fibrosis through tubular cell epithelial-mesenchymal transition (EMT) as well as activation of resident fibroblasts, endothelial-mesenchymal transition (EndoMT) and pericyte-myofibroblast transdifferentiation. Interstitial macrophage infiltration has also been shown to correlate with the severity of kidney fibrosis in various chronic kidney diseases. MMPs secreted by macrophages, especially MMP-9, has been shown by us to be profibrotic by induction of tubular cells EMT. EMT is mainly induced by transforming growth factor-β (TGF-β). However, MMP-9 was found by us and others to be up-regulated by TGF-β1 in kidney tubular epithelial cells and secreted by activated macrophages, resulting in EMT and ultimately kidney fibrosis. Therefore, MMP-9 may serve as a potential therapeutic target to prevent kidney fibrosis in chronic kidney disease. This review, by a particular focus on EMT, seeks to provide a comprehensive understanding of MMPs, especially MMP-9, in kidney fibrosis.
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.
Related Concept Videos
Role of Matrix Metalloproteases in Degradation of ECM
Chronic Kidney Disease I: Introduction
Diabetic Nephropathy
Nephrons
Chronic Kidney Disease III: Interprofessional Care
Renal Corpuscle
Glomerulus: Structure and Function
The glomerulus is a tiny, intricate network of capillaries located at the beginning of the nephron. It's enveloped by the Bowman's capsule and receives its blood supply from an afferent arteriole, which divides into numerous...

