Oxidative stress and transforming growth factor-β1-induced cardiac fibrosis.

A chronic increase in reactive oxygen species (ROS) plays a critical role in the development and progression of cardiac remodeling associated with heart failure. Oxidative stress is indeed increased in heart failure, hypertension, cardiac fibrosis and hypertrophy. In vitro exposure of cardiac fibroblasts to superoxide anion stimulates their proliferation by increasing the production of transforming growth factor-β1 (TGF-β1), a potent fibrogenic cytokine.

Angiotensin II-induced mitochondrial reactive oxygen species and peroxiredoxin-3 expression in cardiac fibroblasts.

Objective: The aim of this study was to determine whether angiotensin II (ANG II) affects the protein and mRNA expression of the mitochondrial antioxidant peroxiredoxin-3 (Prx-3) in cardiac fibroblasts, thereby contributing to the oxidative stress in the myocardium.

Method: Cardiac fibroblasts (passage 2) from normal male adult rats were cultured to confluency and incubated in Dulbecco's modified Eagle's medium for 24  h. The cells were then preincubated with(out) the tested inhibitors for 1  h and further incubated with/without ANG II (1 μmol/l) for 24  h.