Atherosclerosis is the formation of fatty plaques in blood vessel walls, contributing to age-related diseases and mortality. Macrophages play a vital role in cholesterol clearance, but dysfunction leads to plaque development. Research focusing on LDL-cholesterol reduction has shown limited success in reversing plaque. Mitochondrial dysfunction and metabolic reprogramming in macrophages contribute to atherosclerosis progression, affecting plaque morphology. Targeting NOX4-dependent mitochondrial ROS shows promise in managing atherosclerosis. Understanding the mechanisms of macrophage dysfunction and NOX4 activity in aging-related atherosclerosis is crucial for developing effective treatments. In a study using aged mice, inhibiting NOX4 activity preserved mitochondrial function and reduced atherosclerosis progression. The findings highlight the potential of targeting NOX4 or mitochondrial dysfunction to mitigate vascular inflammation and preserve plaque integrity in atherosclerosis.
