Ischemia

Cardiology

Myocardial ischemia

Internal medicine

Medicine

Reperfusion injury

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Despite major progress in interventional and medical treatments, myocardial infarction (MI) and subsequent development of heart failure (HF) are still associated with high mortality. Both during ischemia reperfusion (IR) in the acute setting of MI, as well as in the chronic remodeling process following MI, oxidative stress substantially contributes to cardiac damage. Reactive oxygen species (ROS) generated within mitochondria are particular drivers of mechanisms contributing to IR injury, including induction of mitochondrial permeability transition or oxidative damage of intramitochondrial structures and molecules. But even beyond the acute setting, mechanisms like inflammatory signaling, extracellular remodeling, or pro-apoptotic signaling that contribute to post-infarction remodeling are regulated by mitochondrial ROS. In the current review, we discuss both sources and consequences of mitochondrial ROS during IR and in the chronic setting following MI, thereby emphasizing the potential therapeutic value of attenuating mitochondrial ROS to improve outcome and prognosis for patients suffering MI. • Mitochondrial ROS determines myocardial damage during IR and subsequent remodeling. • Sources of ROS include the ETC, ROS-producing enzymes and impaired detoxification. • Novel mechanisms of ROS include mitochondrial fission and sirtuin dysfunction. • Promising therapies include ROS scavenging and inhibition of mPTP. • Translating attenuation of mitochondrial ROS into humans remains challenging.

Mitochondrial ROS in myocardial ischemia reperfusion and remodeling