Abstract:

[Abstract] Muscle atrophy is a frequent complication of chronic kidney disease (CKD) and is associated with increasing morbidity and mortality. The processes causing loss of muscle mass are also present in several catabolic conditions, such as insulin resistance, acidosis, and inflammation. The main reasons may involve in activation of ubiquitin proteasome pathway (UPP).Three distinct components are required for muscle breakdown using the UPP. E1 ligases which activate ubiquitin, E2 ligases that are responsible for transferring the activated ubiquitin to the protein molecule that is then targeted for degradation and the E3 ligases which regulate the actual transfer of ubiquitin to the protein. Two important skeletal muscle specific ubiquitin E3 ligases are Muscle-specific RING Finger protein 1 (MuRF1) and Muscle Atrophy F-box (MAFbx/atrogin-1), which could be affected by several pathways. Understanding the pathogenesis of CKD-induced muscle loss could lead to therapeutic interventions that prevent muscle wasting in CKD.

Key words: Skeletal muscle atropy, ubiquitin proteasome pathway, Muscle-specific RING