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Published on: November 10, 2021
CTGF and chronic kidney fibrosis
Xin-Ming Chen1, Weier Qi, Carol A Pollock
1Dept of Medicine, Kolling Institute, University of Sydney, Royal North Shore Hospital, Sydney, Australia.
Frontiers in Bioscience (Scholar Edition)
|June 2, 2009
Summary
Connective tissue growth factor (CTGF) drives kidney fibrosis by promoting extracellular matrix imbalance. This review details CTGF's role in diabetic nephropathy, highlighting its interaction with high glucose, angiotensin II, TGF-β1, and AGEs.
Area of Science:
- Nephrology
- Pathology
- Molecular Biology
Background:
- Chronic kidney fibrosis is a hallmark of progressive renal diseases, leading to kidney failure.
- Dysregulation of extracellular matrix production and degradation drives renal fibrosis.
- Connective tissue growth factor (CTGF) has emerged as a key mediator in renal fibrogenesis.
Purpose of the Study:
- To review the role of CTGF in renal fibrosis.
- To elucidate CTGF's specific mechanisms in mediating fibrosis in diabetic nephropathy.
Main Methods:
- Literature review focusing on CTGF's function in renal fibrosis.
- Analysis of CTGF's interactions with key fibrotic factors.
Main Results:
- CTGF promotes cell proliferation, migration, and differentiation, contributing to fibrosis.
- CTGF acts directly or as a co-factor for TGF-β1 in fibrogenesis.
- CTGF modulates factors like VEGF and bone morphogenic proteins involved in renal development and repair.
Conclusions:
- CTGF is a critical factor in the development of renal fibrosis, particularly in diabetic nephropathy.
- Understanding CTGF's profibrotic actions is essential for developing targeted therapies.
- CTGF's interplay with high glucose, angiotensin II, TGF-β1, and AGEs underscores its central role in kidney disease progression.
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