The rapid global aging of the population has heightened the clinical importance of sarcopenia, an interdisciplinary condition characterized by the progressive and widespread decline in skeletal muscle mass, strength, and function. Now formally recognized as a distinct muscle disease, sarcopenia is a key contributor to frailty, physical disability, and increased healthcare use among older adults. While current research encompasses diverse epidemiological and biological perspectives, the integration of multi-system interactions — such as the gut-muscle axis and immune-muscle crosstalk — within clinical assessment remains a vital area of exploration. This review examines the interplay between etiology, molecular pathogenesis, and contemporary diagnostic standards to characterize the syndrome’s complexity. Global prevalence escalates significantly in institutionalized populations or those over age 80. Pathogenesis is rooted in a disruption of protein homeostasis where catabolic pathways, such as the ubiquitin-proteasome system, overwhelm anabolic signaling—a process triggered by mitochondrial dysfunction, chronic low-grade inflammation, and declining sex hormones. Furthermore, the synthesis of diagnostic protocols from international consortia highlights the transition to strength-priority models to better predict the falls, fractures, and cardiovascular events. Despite significant diagnostic progress, more longitudinal research is necessary to refine population-specific cut-off criteria and identify reliable clinical biomarkers. By consolidating current mechanistic evidence and epidemiological trends, this review shows the necessity for the unified diagnostic protocol and calls for continued interdisciplinary research to improve early detection and preserve physical independence in aging societies.
Tsyhanyk et al. (2026) studied this question.