The age-related loss of skeletal muscle function starts from midlife and if left unaddressed can lead to an impaired quality of life. A growing body of evidence indicates that mitochondrial dysfunction is causally involved with muscle aging. Muscles are tissues with high metabolic requirements, and contain rich mitochondria supply to support their continual energy needs. Cellular mitochondrial health is maintained by expansing of the mitochondrial pool though mitochondrial biogenesis, by preserving the natural mitochondrial dynamic process, via fusion and fission, and by ensuring the removal of damaged mitochondria through mitophagy. During aging, mitophagy levels decline and negatively impact skeletal muscle performance. Nutritional and pharmacological approaches have been proposed to manage the decline in muscle function due to impaired mitochondria bioenergetics. The natural postbiotic Urolithin A has been shown to promote mitophagy, mitochondrial function and improved muscle function across species in different experimental models and across multiple clinical studies. In this review, we explore the biology of Urolithin A and the clinical evidence of its impact on promoting healthy skeletal muscles during age-associated muscle decline.

与年龄相关的骨骼肌功能丧失从中年开始，如果不加以解决，可能会导致生活质量受损。越来越多的证据表明线粒体功能障碍与肌肉衰老有关。肌肉是代谢需求较高的组织，含有丰富的线粒体供应来支持其持续的能量需求。细胞线粒体的健康是通过线粒体生物发生扩大线粒体池、通过融合和裂变保留自然线粒体动态过程以及通过线粒体自噬确保去除受损线粒体来维持的。在衰老过程中，线粒体自噬水平下降并对骨骼肌性能产生负面影响。已经提出了营养和药理学方法来控制由于线粒体生物能受损而导致的肌肉功能下降。在不同的实验模型和多项临床研究中，天然后生元尿石素 A 已被证明可以促进线粒体自噬、线粒体功能和改善跨物种的肌肉功能。在这篇综述中，我们探讨了尿石素 A 的生物学特性及其在与年龄相关的肌肉衰退期间促进骨骼肌健康的影响的临床证据。