Reduced nitric oxide bioavailability drives cardiovascular aging, while interventions like dietary nitrate supplementation, caloric restriction, and exercise may restore signaling and counteract decline.
Nitric oxide (NO) is essential for maintaining normal cardiovascular function, and accumulating evidence suggests that its diminished bioavailability contributes to endothelial dysfunction, vascular stiffening, and impaired cardiac performance - hallmarks of cardiovascular aging. This review posits that reduced NO bioavailability with age stems from impaired endothelial and neuronal NO synthase activity, increased oxidative stress, and metabolic shifts that drive cardiovascular decline. We further discuss emerging research which highlights potential interventions, including dietary nitrate supplementation, caloric restriction, and exercise, that may restore NO signaling and counteract age-related cardiovascular dysfunction. These findings underscore the growing recognition of NO as a key regulator of cardiovascular aging and a promising therapeutic target. Addressing NO-related deficits could open new avenues for preventing and treating age-associated cardiovascular diseases, reshaping strategies for promoting healthy aging and longevity.
Adhikari et al. (Mon,) conducted a review in Cardiovascular aging. Dietary nitrate supplementation, caloric restriction, and exercise was evaluated. Reduced nitric oxide bioavailability drives cardiovascular aging, while interventions like dietary nitrate supplementation, caloric restriction, and exercise may restore signaling and counteract decline.