Mitochondria regulate cardiac energy metabolism, calcium buffering, reactive oxygen species (ROS) signaling, and programmed cell death, playing a vital role in maintaining heart function and its response to physiological stress. Disruptions in mitochondrial quality control, dynamics, and metabolic signaling contribute fundamentally to the pathogenesis of heart failure, ischemic injury, cardiomyopathy and atrial fibrillation. Over the past five years, growing evidence has linked mitochondrial dysfunction to many cardiac pathologies, spurring research into five key areas: (1) molecular mechanisms, (2) mitochondrial biomarkers, (3) mitochondria-targeted therapies, (4) disease-specific insights, and (5) clinical trials. Below we summarize recent scientific and clinical progress in each area, highlighting emerging mechanisms and especially promising therapeutic directions.
Wang et al. (Tue,) studied this question.