LXR/CD38 activation drives cholesterol-induced macrophage senescence and neurodegeneration via NAD+ depletion

Terao et al. demonstrated how dysregulated cholesterol metabolism drives macrophage senescence and the development of subretinal drusenoid deposits in mice. LXR/CD38 signaling activated by cholesterol reduces NAD+ availability and promotes macrophage senescence. Senolytic agents targeting NAD+ decline and senescent macrophages are a potential therapeutic option against early AMD.

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