Ventricular differences in mitochondrial Ca2+ dynamics in murine and porcine hearts
In cardiomyocytes, mitochondria produce ~95% of the ATP required for contraction [1]. Mitochondrial Ca2+ (mtCa2+) activates matrix-localized enzymes and helps to match ATP production to demand. However, mtCa2+ overload can lead to reactive oxygen species (ROS) generation and opening of the mitochondrial permeability transition pore (mPTP), which induces cell death [1,2]. Preventing mPTP opening might be a therapeutic target for cardiovascular diseases, including right ventricle (RV) failure in pulmonary hypertension [3].
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Jae Hwi Sung, Hector Chapoy Villanueva, Feng Feng, Ariadna Araque Igualador, Kurt W. Prins, Julia C. Liu Tags: Letter to the editor Source Type: research
More News: Cardiology | Cardiovascular | Cytology | Heart | Hypertension | Mitochondria | Mitochondrial Disease | Pulmonary Hypertension