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This study demonstrates that periodic exposure to red light can mitigate aging in mice by enhancing histone H3 Lys9 acetylation (H3K9ac) through the modulation of fatty acid metabolism. Red light exposure reduces SIRT4 protein levels in keratinocytes, which activates glycolysis, fatty acid metabolism, and the TCA cycle. The decrease in SIRT4 enhances mitochondrial fatty acid oxidation and activates SIRT1, which in turn alleviates inhibition on PPAR-α, leading to increased expression of lipid metabolism-related genes. This results in the accumulation of acetyl-CoA, increased H3K9ac levels, and altered expression of senescence-related genes, effectively reducing cellular aging through coordinated regulation of metabolism, inflammation, and gene expression.

This study demonstrates that periodic exposure to red light can mitigate aging in mice by enhancing histone H3 Lys9 acetylation (H3K9ac) through the modulation of fatty acid metabolism. Red light exposure reduces SIRT4 protein levels in keratinocytes, which activates glycolysis, fatty acid metabolism, and the TCA cycle. The decrease in SIRT4 enhances mitochondrial fatty acid oxidation and activates SIRT1, which in turn activates PPAR-α, leading to increased expression of lipid metabolism-related genes. This results in the accumulation of acetyl-CoA, increased H3K9ac levels, and altered expression of senescence-related genes, effectively reducing cellular aging through coordinated regulation of metabolism, inflammation, and gene expression.

This study investigates the role of ACOD1 in androgenetic alopecia (AGA), highlighting its impact on dermal papilla cell (DPC) senescence. The research shows that ACOD1 deficiency leads to increased DDX1 methylation, resulting in mitochondrial dysfunction and DPC senescence, which are key factors in AGA pathogenesis. The study utilized various methods, including RNA sequencing and metabolomic analysis, to demonstrate that ACOD1 knockdown exacerbates mitochondrial issues and cellular aging, while its overexpression mitigates these effects. Additionally, the study found that exogenous 4-octyl itaconate (4-OI) supplementation can reduce DDX1 methylation, improve mitochondrial function, enhance cell proliferation, and reduce hair loss in AGA mice. These findings suggest that targeting ACOD1 and using 4-OI could be promising therapeutic strategies for treating AGA.