Abstract
After spinal cord injury(SCI),the myelin debris resulting from axonal collapse is considered as a significant impediment to nerve regeneration.The removal of myelin debris is crucial to establish a favorable microenvironment for nerve regeneration.Macrophages play a pivotal role in this clearance process.However,following phagocytosis,the lipid levels within macrophages increase significantly,leading to disrupted lipid metabolism and eventual foam cell formation.This proinflammatory type of foamy macrophage is unable to transition to the anti-inflammatory phenotype which is necessary for repair.Consequently,the lesion area remains stuck in the inflammatory phase for an extended period,hampering the post-SCI repair process.We reviewed the connection and mechanisms between lipid metabolism and inflammatory phenotype of macrophages after SCI.Furthermore,we discussed potential lipid metabolism-related genes that could facilitate repair,offering a novel strategy for SCI treatment.
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