Muscle Wasting: Molecular Mechanisms and Promising Therapies

Abstract

Muscle atrophy, often known as muscle wasting, is a severe disorder marked by a decrease of skeletal muscle mass and strength. It occurs in various pathological states, including chronic kidney disease, cancer, chronic obstructive pulmonary disease (COPD), and heart failure, as well as during extended periods inactivity or aging. Muscle wasting is caused by an imbalance between the production and degradation of proteins, and important regulators including the autophagy-lysosomal pathway, ubiquitin-proteasome system (UPS), and inflammatory cytokines are crucial in this process. Muscle homeostasis is regulated by important signaling pathways, such as the Akt/mTOR and NF-κB pathways. Furthermore, oxidative stress and mitochondrial dysfunction make muscle deterioration worse. By focusing on these molecular pathways, new treatment approaches seek to prevent muscle wasting. Preclinical and clinical investigations have demonstrated the potential of pharmacological treatments, including myostatin inhibitors, anti-inflammatory drugs, and anabolic agents, as well as nutritional therapies and regular exercise. New approaches to muscle regeneration are provided by emerging medicines such as RNA-based methods, gene editing, and stem cell therapy. This study examines the complex molecular processes causing muscle wasting and identifies effective treatment approaches meant to maintain muscular mass and function. Understanding these mechanisms is essential for developing effective treatments that enhance the quality of life for those affected.