{Reference Type}: Journal Article
{Title}: Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.
{Author}: Dridi H;Santulli G;Bahlouli L;Miotto MC;Weninger G;Marks AR;
{Journal}: Biomolecules
{Volume}: 13
{Issue}: 9
{Year}: 2023 09 19
{Factor}: 6.064
{DOI}: 10.3390/biom13091409
{Abstract}: Heart failure is a serious global health challenge, affecting more than 6.2 million people in the United States and is projected to reach over 8 million by 2030. Independent of etiology, failing hearts share common features, including defective calcium (Ca2+) handling, mitochondrial Ca2+ overload, and oxidative stress. In cardiomyocytes, Ca2+ not only regulates excitation-contraction coupling, but also mitochondrial metabolism and oxidative stress signaling, thereby controlling the function and actual destiny of the cell. Understanding the mechanisms of mitochondrial Ca2+ uptake and the molecular pathways involved in the regulation of increased mitochondrial Ca2+ influx is an ongoing challenge in order to identify novel therapeutic targets to alleviate the burden of heart failure. In this review, we discuss the mechanisms underlying altered mitochondrial Ca2+ handling in heart failure and the potential therapeutic strategies.