Urolithin A is one of a number of compounds available as supplements that can improve mitochondrial function in older individuals. Like others, urolithin A may function by improving the mitochondrial quality control process of mitophagy, responsible for removing damaged and worn mitochondria. Mitophagy becomes less efficient with age, and this is one of the contributing factors to age-related loss of mitochondrial function and its harmful impact on tissues. Like other supplement based approaches to improving mitochondrial function, it is likely that regular exercise delivers larger gains than those demonstrated for supplementation with urolithin A. Whether exercise and supplementation produce greater gains when undertaken in combination is poorly studied, unfortunately.
Cardiovascular diseases remain the primary cause of global mortality, necessitating effective strategies to alleviate their burden. Mitochondrial dysfunction is a driving force behind aging and chronic conditions, including heart disease. Here, we investigate the potential of Urolithin A (UA), a gut microbiome-derived postbiotic that enhances mitophagy, to ameliorate both age-related decline in cardiac function and cardiac failure.
We highlight the significance of targeting mitochondria, by comparing gene expression changes in aging human hearts and cardiomyopathies. UA oral administration successfully counteracts mitochondrial and cardiac dysfunctions in preclinical mouse models of aging and heart failure. In mice, UA improves both systolic and diastolic heart functions, distinguishing it from other mitochondrial interventions. In cardiomyocytes, UA recovers mitochondrial ultrastructural defects and decline in mitochondrial biomarkers occurring with aging and disease. These findings extend UA's benefits to heart health, making UA a promising nutritional intervention to evaluate in the clinic to promote healthy cardiovascular function as we age.