Simultaneous targeting of oxidative stress and fibrosis as an effective strategy for treating cardiomyopathy-induced ventricular remodelling and dysfunction

Chrishan Samuel

This presentation outlines the background to why the therapeutic targeting of the interaction between transforming growth factor (TGF)-beta1 and oxidative stress would provide an effective means of reducing tissue remodelling-induced fibrosis progression and related dysfunction.
It also provides evidence from in vitro and in vivo studies conducted to demonstrate how the targeting of this interaction between TGF-beta1 and oxidative stress can effectively reduce left ventricular inflammation, remodelling and fibrosis, as well as cardiomyocyte hypertrophy and left ventricular dysfunction in a preclinical model of cardiomyopathy-induced fibrosis.
These findings have important implications for developing new drugs or repurposing currently-available drugs to target this TGF-beta1oxidative stress interaction.

 

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