Journal Article

Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection

Bertero, Edoardo, Popoiu, Tudor-Alexandru, Maack, Christoph

2024

Overview

Mitochondrial calcium (Ca2+) signals play a central role in cardiac homeostasis and disease. In the healthy heart, mitochondrial Ca2+ levels modulate the rate of oxidative metabolism to match the rate of adenosine triphosphate consumption in the cytosol. During ischemia/reperfusion (I/R) injury, pathologically high levels of Ca2+ in the mitochondrial matrix trigger the opening of the mitochondrial permeability transition pore, which releases solutes and small proteins from the matrix, causing mitochondrial swelling and ultimately leading to cell death. Pharmacological and genetic approaches to tune mitochondrial Ca2+ handling by regulating the activity of the main Ca2+ influx and efflux pathways, i.e., the mitochondrial Ca2+ uniporter and sodium/Ca2+ exchanger, represent promising therapeutic strategies to protect the heart from I/R injury.

• Publisher: Springer Nature B.V
• Subject: Adenosine diphosphate / Adenosine triphosphate / Calcium (mitochondrial) / Calcium efflux / Calcium homeostasis / Calcium influx / Calcium ions / Calcium metabolism / Calcium permeability / Calcium signalling / Cardiology / Cell death / Coronary artery disease / Cytosol / Efflux / Heart diseases / Heart failure / Heart rate / Homeostasis / Injuries / Investigations / Ischemia / Membrane permeability / Metabolism / Mitochondria / Mitochondrial DNA / Mitochondrial permeability transition pore / Oxidation / Oxidative metabolism / Permeability / Phosphorylation / Physiology / Proteins / Protons / Reperfusion / Solutes / Workloads