Efectos de la suplementación con Urolitina A sobre la regulación de la homeostasis mitocondrial e inflamación como estrategia para mejorar la salud muscular durante el envejecimiento

Abstract

During aging, there is a progressive decrease in skeletal muscle functionality, associated with an increased risk of falls and fractures, frailty, loss of mobility, and loss of independence. Current studies have shown that physical activities and nutritional interventions delay the progression of aging and prevent a decline in functionality. Thus, studies have examined the effects of Urolithin A (UA) supplementation, a natural compound produced by the gut microbiota through dietary polyphenols. In older adults, among the factors that lead to the reduction of muscle mass and function in this population are: 1) mitochondrial homeostasis alterations, loss of the capacity to remove damaged mitochondria (mitophagy), and 2) age-associated systemic inflammation (inflamm-aging) leading to a release of proinflammatory cytokines through activation of inflammatory signaling pathways, such as NF-kB and cGAS/STING. The evidence suggests that UA stimulates mitophagy and has a regulatory effect on skeletal muscle inflammation in older adults. Currently, it is known that physical activity could improve mitochondrial homeostasis and decrease inflammation. To date, there are no clinical trials combining the UA with physical activity in this population. This review aims to show the most recent literature on the clinical relevance of UA supplementation on the regulation of systemic inflammation associated with altered mitochondrial homeostasis as a strategy to improve muscle function and quality of life of older adults. Furthermore, to project future strategies for possible applications to combine UA supplementation with physical activity.