Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart

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.

The Roles of CircRNAs in Mitochondria

“…However, the capacity for Ca 2+ of mitochondria is finite. The overload of Ca 2+ may lead to produce reactive oxygen species and ultimately lead to cell death 54 .…”

Micronutrient Status and Breast Cancer: A Narrative Review

“…Krebs cycle stimulation is dependent on Ca 2+ concentration in the mitochondria, and the products of this metabolic reaction, FADH2 and NADH, supply electrons to the electron transport chain. In hypoxemic conditions, an elevated number of electrons released in electron transport chain may transfer to molecular oxygen, forming superoxide anions, which are harmful to the surrounding cells [213][214][215]. Both processes, in which Ca plays an important role, may contribute to an increased risk of carcinogenesis.…”