期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/ijms22095009
关键词
axonal regeneration; lipid rafts; cholesterol; sphingolipid; CNS injury; neurodegeneration; axonal growth-inhibitory molecules
资金
- Spanish MINECO [SAF2016-76340R, PID2019-106764RB-C21]
- CIBERNED (ISCIII)
- Spanish MECD [FPU14/02156, BES-2014-067857]
- TERCEL [RD12/0019/0011]
- Generalitat de Catalunya [2014SGR1609]
- Clem Jones Foundation
- State Government of Queensland
- NHMRC Boosting Dementia Research Initiative
- MECD [FPU14/02156, 2014-067857]
- ERDF funds
Central nervous system damage from various causes is a major worldwide contributor to physical disability. The limited ability of the adult nervous system to heal and regenerate after injury has prompted research into therapies to enhance axonal regeneration. Recent findings suggest a link between the stability and composition of lipid rafts and the capacity of axons to rebuild functional neural circuits after damage.
Central nervous system damage caused by traumatic injuries, iatrogenicity due to surgical interventions, stroke and neurodegenerative diseases is one of the most prevalent reasons for physical disability worldwide. During development, axons must elongate from the neuronal cell body to contact their precise target cell and establish functional connections. However, the capacity of the adult nervous system to restore its functionality after injury is limited. Given the inefficacy of the nervous system to heal and regenerate after damage, new therapies are under investigation to enhance axonal regeneration. Axon guidance cues and receptors, as well as the molecular machinery activated after nervous system damage, are organized into lipid raft microdomains, a term typically used to describe nanoscale membrane domains enriched in cholesterol and glycosphingolipids that act as signaling platforms for certain transmembrane proteins. Here, we systematically review the most recent findings that link the stability of lipid rafts and their composition with the capacity of axons to regenerate and rebuild functional neural circuits after damage.
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