title: The molecular mechanisms of calpains action on skeletal muscle atrophy.
abstract: Skeletal muscle atrophy is associated with a loss of muscle protein which may result from both increased proteolysis and decreased protein synthesis. Investigations on cell signaling pathways that regulate muscle atrophy have promoted our understanding of this complicated process. Emerging evidence implicates that calpains play key roles in dysregulation of proteolysis seen in muscle atrophy. Moreover, studies have also shown that abnormally activated calpain results muscle atrophy via its downstream effects on ubiquitin-proteasome pathway (UPP) and Akt phosphorylation. This review will discuss the role of calpains in regulation of skeletal muscle atrophy mainly focusing on its collaboration with either UPP or Akt in atrophy conditions in hope to stimulate the interest in development of novel therapeutic interventions for skeletal muscle atrophy.
authors.affiliation: Ningxia Medical University, Yinchuan, Ningxia, China; Department of Respiratory Diseases, YangPu Hospital of Tongji University, Shanghai, China. z_xping@hotmail.com.
authors.forename: Jiaru
authors.initials: J
authors.lastname: Huang
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Zhu
mesh_terms: D000818:Animals; D002154:Calpain / Q000378:metabolism*; D006801:Humans; D006984:Hypertrophy; D009124:Muscle Proteins / Q000378:metabolism*; D009133:Muscular Atrophy / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D059748:Proteolysis; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D020239:Receptor Cross-Talk; D015398:Signal Transduction; D025801:Ubiquitin / Q000378:metabolism
chemical_list: D009124:Muscle Proteins; D025801:Ubiquitin; D051057:Proto-Oncogene Proteins c-akt; D002154:Calpain; D046988:Proteasome Endopeptidase Complex; C061553:ATP dependent 26S protease