Please use this identifier to cite or link to this item: https://doi.org/10.4103/1673-5374.317956
Title: Cholesterol synthesis inhibition or depletion in axon regeneration
Authors: Tang, Bor Luen 
Keywords: axon regeneration
cholesterol
3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase)
lipid raft
methyl-β-cyclodextrin
Nogo receptor
prominin-1
RhoA
statin
Issue Date: 1-Feb-2022
Publisher: WOLTERS KLUWER MEDKNOW PUBLICATIONS
Citation: Tang, Bor Luen (2022-02-01). Cholesterol synthesis inhibition or depletion in axon regeneration. NEURAL REGENERATION RESEARCH 17 (2) : 271-276. ScholarBank@NUS Repository. https://doi.org/10.4103/1673-5374.317956
Abstract: Cholesterol is biosynthesized by all animal cells. Beyond its metabolic role in steroidogenesis, it is enriched in the plasma membrane where it has key structural and regulatory functions. Cholesterol is thus presumably important for post-injury axon regrowth, and this notion is supported by studies showing that impairment of local cholesterol reutilization impeded regeneration. However, several studies have also shown that statins, inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase, are enhancers of axon regeneration, presumably acting through an attenuation of the mevalonate isoprenoid pathway and consequent reduction in protein prenylation. Several recent reports have now shown that cholesterol depletion, as well as inhibition of cholesterol synthesis per se, enhances axon regeneration. Here, I discussed these findings and propose some possible underlying mechanisms. The latter would include possible disruptions to axon growth inhibitor signaling by lipid raft-localized receptors, as well as other yet unclear neuronal survival signaling process enhanced by cholesterol lowering or depletion.
Source Title: NEURAL REGENERATION RESEARCH
URI: https://scholarbank.nus.edu.sg/handle/10635/234799
ISSN: 1673-5374
1876-7958
DOI: 10.4103/1673-5374.317956
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