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Muscle tissue proteolysis pathway encompasses several tightly regulated molecular mechanisms responsible for the breakdown of muscle proteins into peptides and amino acids, ensuring proper muscle cell function, adaptation, and homeostasis. The dominant systems include the ubiquitin-proteasome pathway (tagging proteins for degradation via ubiquitination and subsequent destruction by the 26S proteasome)[1][2][4], autophagy-lysosome pathway (recycling organelles and large proteins)[1][4], calpain system (calcium-dependent proteases), and caspase pathway (involved in apoptosis)[1][4]. Dysregulation leads to pathologic muscle wasting and atrophy, which is central to chronic diseases, disuse, aging, and various myopathies[1][3][4]. Direct intervention in the entire pathway is impossible; instead, research and therapeutic strategies focus on specific pathway components, mainly ubiquitin ligases (Atrogin-1, MuRF1) and the regulation of PI3K/AKT/mTOR signaling[3][4][1][2].
Inhibition of protein degradation (proteasome inhibitors); Blockade of E3 ubiquitin ligase function; Modulation of signaling pathways (IGF-1 analogs to activate PI3K/AKT, suppressing atrophy genes); Stimulation of protein synthesis; Other
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