Pharmacological targeting of mitochondrial reactive oxygen species counteracts diaphragm weakness in chronic heart failure

Chronic heart failure (CHF) heightens intact mitochondria H2O2 emission and weakens the diaphragm. Systemic treatment with a mitochondria-targeted antioxidant, starting once CHF was already established, normalized diaphragm mitochondrial H2O2 emission and contractile function. The effects of mitochondria-targeted antioxidant treatment were associated with the maintenance of diaphragm glutathione content. Thus antioxidant strategies specifically targeting the mitochondria could therapeutically benefit respiratory function in CHF.