Furthermore, increased ROS production by TGF-β 1 is correlated with increased activity of NAD (P) H oxidase and expression of membrane subunits of the NAD (P) H oxidase complex.
The effects of TGF-β 1 on myocyte function are abolished by NAD (P) H oxidase inhibitors and by exogenous GSH and N -acetylcysteine (NAC), a precursor of GSH.