Autophagy and oxidative stress influence cardiovascular pathology. Autophagy mediates lysosome-dependent clearance of damaged proteins and organelles and maintains mitochondrial quality control, proteostasis, and metabolic flexibility. Reactive oxygen species (ROS) originate from mitochondrial respiration and enzymatic reactions during stress. At physiological levels, ROS function as redox signals that activate degradation and recycling, whereas excess oxidants damage lipids, proteins, and nucleic acids and promote cell loss. This review integrates evidence across cardiovascular disease, including atherosclerosis, ischemia reperfusion injury, pressure overload remodeling, heart failure, diabetic cardiomyopathy, arrhythmia, aging, and inflammation.
Yun et al. (2025) studied this question.