IMR Press / FBS / Volume 1 / Issue 1 / DOI: 10.2741/S13

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

CTGF and chronic kidney fibrosis
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1 Dept of Medicine, Kolling Institute, University of Sydney, Royal North Shore Hospital, Sydney, Australia
2 Dept of Medicine, University of Melbourne, St Vincent's Hospital, Melbourne, Australia

*Author to whom correspondence should be addressed.

Academic Editor: Youhua Liu

Front. Biosci. (Schol Ed) 2009, 1(1), 132–141;
Published: 1 June 2009
(This article belongs to the Special Issue New insights into the pathogenesis and therapeutics of renal fibrosis)

Chronic kidney fibrosis is the unifying pathological feature of diverse renal disease leading to a progressive decline in renal function and eventually end-stage kidney failure. Many growth factors are able to induce an imbalance of extracellular matrix production and degradation, leading to excessive matrix and fibrosis in both glomeruli and in the tubulointerstitium. Over the last decade the role of connective tissue growth factor (CTGF) in renal fibrosis has been intensively studied. CTGF participates in cell proliferation, migration, and differentiation and mediates profibrotic activity by acting either directly, or as a co-factor for TGFβ1, which is well characterised as a key cytokine mediating both the induction and promotion of fibrogenesis. CTGF also has the potential to modulate factors such as VEGF and bone morphogenic proteins, which are integral to both the development and repair process inherent in renal fibrogenesis. This review focuses on the role of CTGF in renal fibrosis and specifically its role in inducing fibrosis by factors integrally involved in the development of diabetic nephropathy, namely high glucose, angiotensin II, TGFβ1 and AGEs.

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