Sarcopenia: Relevance, Epidemiology, Etiopathogenesis, Histological Characteristics, and Modern Treatment Approaches

Abstract

The study aimed to conduct a comprehensive theoretical analysis of modern concepts regarding the etiopathogenesis and pathomorphological mechanisms of sarcopenia development. The goal was to update the understanding of the systemic and generalized nature of this condition as a multisystem disorder affecting skeletal muscles and integrated body systems. An information search was performed across major databases, including PubMed, Scopus, Embase, Web of Science, and Google Scholar. The study analyzed sources published between 2016 and 2026, focusing on the pathomorphological mechanisms, classification, and methods of correction for sarcopenia. Sarcopenia is identified as a multifactorial state characterized by a transition from healthy muscle architecture to qualitative degradation. Key findings include: Sarcopenia is divided into primary (age-related) and secondary (associated with chronic diseases, such as heart failure or HIV, and lifestyle factors). The condition involves selective atrophy of Type II (fast-twitch) muscle fibers, while Type I fibers remain relatively intact. Pathogenesis includes myosteatosis (fatty infiltration) driven by fibro-adipogenic progenitors (FAPs), myofibrosis (excessive collagen synthesis), and the fragmentation of neuromuscular junctions (NMJ). A critical decline in the number and proliferative potential of satellite cells (MuSCs) prevents effective muscle repair. Systemic inflammation ("inflammaging"), oxidative stress, and hormonal imbalances (deficit of IGF-1 and anabolic hormones) drive the catabolic shift. Sarcopenia is a complex, systemic disease that extends far beyond simple age-related muscle loss. It represents a profound structural and functional degradation characterized by fiber atrophy, fatty and fibrous replacement, and impaired neuromuscular transmission. Effective clinical management requires a multisystemic approach that targets molecular and cellular mechanisms alongside lifestyle and nutritional interventions.