From Sarcopenia to Frailty: The Pathophysiological Basis and Potential Target Molecules of Intervention

Abstract

Skeletal muscle is not only an endocrine organ but also one of core components of mus-closkeletal system. Sarcopenia refers to a decline in the skeletal muscle mass and func-tion. The former involves the size and number of changes in two types of myofibers, lower satellite cell density, and regeneration ability. The latter shows a loss of muscle strength. Frailty is a geriatric syndrome with multisystem impairment associated with increased vulnerability to stressors. Sarcopenia increases the risk of frailty and may be one of the major causes of physical frailty phenotype. Sarcopenia is also potentially asso-ciated with cognitive frailty phenotype. Aging might be the common underlying patho-physiology of sarcopenia and frailty. Therefore, there are some potential target molecules in aging-related signaling pathways that might be associated with sarcopenia and frailty. Nevertheless, sarcopenia can mediate metabolism and promote accelerate systemic aging, frailty, and age-related diseases by myokines in an endocrine manner. Lifestyle interventions (resistance exercise and dietary restriction) of gerontoscience are effective in the prevention of sarcopenia. Some pharmacological agents are registered in different phases of clinical trials for sarcopenia intervention. Phytochemicals, mTOR inhibitors, metformin and acarbose, NAD precursors, and sirtuin activators demonstrated that mul-tiple target antiaging effects might also have preventive and therapeutic perspectives on sarcopenia and frailty.