title: PI3 Kinase regulation of neural regeneration and muscle hypertrophy after spinal cord injury.
abstract: Spinal cord injury (SCI) is a serious neurotrauma that can lead to life-long disability; to date, no suitable therapeutic strategy exists. Axons do not regenerate after SCI in adult mammals and loss of skeletal muscle mass occurs very rapidly after SCI. Promotion of neurite growth through improving the extracellular environment allows only a limited degree of axon regeneration. The phosphatidylinositol-3 kinase (PI3K)/Akt pathway and its downstream targets ("mammalian target of rapamycin," mTOR, and glycogen synthase kinase-3), which regulate cell growth and proliferation in many tissues, have been suggested to play an important role in regulation of the intrinsic axonal regeneration and muscle hypertrophy. This review is focused on recent progress in our understanding of the PI3K pathway in the modulation of axonal regeneration and muscle hypertrophy after SCI.
authors: Department of Orthopedics Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Jiefang Road 88#, Hangzhou, 310009, People's Republic of China.
authors: Tengfei
authors: T
authors: Zhao
authors: Yiying
authors: Y
authors: Qi
authors: Yan
authors: Y
authors: Li
authors: Kan
authors: K
authors: Xu
mesh_terms: D000818:Animals; D006801:Humans; D006984:Hypertrophy; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000473:pathology* / Q000503:physiopathology; D009416:Nerve Regeneration / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D015398:Signal Transduction; D013119:Spinal Cord Injuries / Q000201:enzymology* / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy
chemical_list: D019869:Phosphatidylinositol 3-Kinases