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This remodeling was accompanied by upregulated expression patterns in microglia, astrocytes, and oligodendrocyte precursor cells, suggesting that plasticity mediated by central glial cells may represent an important mechanism underlying NPP (123)

Increases SIRT-1 activity as a result of enhanced NAD+ salvage, leading to beneficial epigenetic and metabolic reprogramming, including increased oxidative phosphorylation (OXPHOS) and muscle stem cell activation 1-3

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Ferroptosis promotes the development of AS through inflammation, endothelial cell dysfunction, and the formation of foam cells, using ferroptosis inhibitors in AS could reverse these effects, which may provide new targets and strategies for the prevention and treatment of AS

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