Mitochondria play a critical role in maintaining the bioenergetic status of cells under physiological conditions. However, reduction of oxygen to generate free radicals occurs at various sites in the mitochondrial respiratory chain, affecting the availability of key regulators of vascular homeostasis. Indeed, several studies suggest that mitochondrial-derived reactive oxygen species (ROS) are involved in endothelial dysfunction, which triggers the development and progression of atherosclerosis in aging individuals and animal models. Among the potential mechanisms underlying age-related impairment of endothelial function, reduction of nitric oxide (NO) bioavailability due to its reaction with oxygen-derived free radicals plays a pivotal role. The present article focuses on the pathophysiology of vascular senescence and explores the interactions of ROS and NO pathways relevant to cardiovascular aging.
- Endothelial dysfunction
- Nitric oxide
- Oxidative stress
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine