The GSK3β pathway in optic nerve regeneration
Research output: Contribution to journal › Article › peer-review
Colleges, School and Institutes
Adult neurons in the mammalian central nervous system (CNS) fail to regenerate after injury due to a number of factors including the reduced intrinsic growth capacity together with the hostile environment of the injured CNS microenvironment [1-4]. However recent studies have shown that modifying the intrinsic growth capacity through a number of cell signalling pathways can promote regeneration of adult CNS neurons. For example, intrinsic factors such as cyclic adenosine monophosphate (cAMP), mammalian target of rapamycin (mTOR), and the repressors phosphatase and tensin homolog (PTEN) and suppressor of cytokine signalling 3 (SOCS3) promote CNS axon regeneration [5-7]. The observation that cAMP and mTOR activity are developmentally downregulated and new protein synthesis is suppressed after mTOR inactivation probably explains why some axons do not normally regenerate in the mature CNS.
|Number of pages||7|
|Journal||Archives of Clinical and Experimental Ophthalmology|
|Publication status||Published - 14 Jul 2020|