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. 2005 Feb 15;65(3):694-701.
doi: 10.1016/j.cardiores.2004.10.041.

Tranilast attenuates cardiac matrix deposition in experimental diabetes: role of transforming growth factor-beta

Jennifer Martin  1 , Darren J Kelly, Sally A Mifsud, Yuan Zhang, Alison J Cox, Fiona See, Henry Krum, Jennifer Wilkinson-Berka, Richard E Gilbert
Affiliations

Tranilast attenuates cardiac matrix deposition in experimental diabetes: role of transforming growth factor-beta

Jennifer Martin et al. Cardiovasc Res. .

Abstract

Objective: The pathological accumulation of extracellular matrix is a characteristic feature of diabetic cardiomyopathy that is directly related to a loss of function. Tranilast (n-[3,4-anthranilic acid), used for the treatment of fibrotic skin diseases, has also been shown to inhibit transforming growth factor-beta (TGF-beta)-induced matrix production in kidney epithelial cells.

Methods: To investigate the effects of tranilast in the diabetic heart, we examined its effects in cultured cardiac fibroblasts and then assessed its effects in (mRen-2)27 diabetic rats with established disease (8 weeks after streptozotocin).

Results: In vitro studies demonstrated a 58% reduction in TGF-beta1-induced 3[H]-hydroxyproline incorporation with tranilast 30 microM (p<0.01). At 16 weeks, diabetes in the Ren-2 rat was associated with increased cardiac fibrosis and evidence of TGF-beta1 activation, as measured by the abundance of phosphorylated Smad2. Despite persistent hyperglycaemia and hypertension, tranilast attenuated cardiac fibrosis by 37% (p<0.05) in association with reduction in phospho-Smad2 (p<0.01).

Conclusion: These findings indicate that tranilast has antifibrotic actions in the Ren-2 model of experimental diabetic cardiac disease by mechanisms that might attributable to reduced TGF-beta activity.

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