This paper reviews the cellular and molecular mechanisms underlying muscle atrophy, a condition characterized by the loss of muscle mass and function. Muscle atrophy is associated with poor prognosis in various diseases, including myopathies, muscular dystrophies, and systemic disorders such as cancer, diabetes, sepsis, and heart failure. The review focuses on the ubiquitin-proteasome system and the autophagy-lysosome system, which are key proteolytic pathways involved in muscle protein turnover. The ubiquitin-proteasome system is activated during muscle atrophy, leading to the degradation of contractile proteins and organelles. The autophagy-lysosome system plays a crucial role in the turnover of cell components, including the selective removal of specific organelles like mitochondria through mitophagy. The paper also discusses the signaling pathways that regulate muscle atrophy, including the IGF1-Akt-FoxO pathway, myostatin, NFκB, and glucocorticoids. These pathways coordinate protein synthesis and degradation, and their dysregulation can contribute to muscle atrophy. Understanding these mechanisms provides new therapeutic targets for preventing and treating muscle atrophy in metabolic and neuromuscular diseases.This paper reviews the cellular and molecular mechanisms underlying muscle atrophy, a condition characterized by the loss of muscle mass and function. Muscle atrophy is associated with poor prognosis in various diseases, including myopathies, muscular dystrophies, and systemic disorders such as cancer, diabetes, sepsis, and heart failure. The review focuses on the ubiquitin-proteasome system and the autophagy-lysosome system, which are key proteolytic pathways involved in muscle protein turnover. The ubiquitin-proteasome system is activated during muscle atrophy, leading to the degradation of contractile proteins and organelles. The autophagy-lysosome system plays a crucial role in the turnover of cell components, including the selective removal of specific organelles like mitochondria through mitophagy. The paper also discusses the signaling pathways that regulate muscle atrophy, including the IGF1-Akt-FoxO pathway, myostatin, NFκB, and glucocorticoids. These pathways coordinate protein synthesis and degradation, and their dysregulation can contribute to muscle atrophy. Understanding these mechanisms provides new therapeutic targets for preventing and treating muscle atrophy in metabolic and neuromuscular diseases.