Red light lowered SIRT4 in aged mice and raised H3K9ac in their tissues
In aged mice, periodic red light exposure was reported to reduce SIRT4 in keratinocytes, activate fatty acid metabolism and raise H3K9ac in tissues; the abstract describes cellular aging as mitigated. [1]
Automatic summary · not editorially reviewed
The key findings
In aged mice, periodic red light exposure was reported to significantly increase H3K9ac levels in tissues and organs. [1]
After red light exposure, SIRT4 protein in keratinocytes was notably reduced, while glycolysis, fatty acid metabolism and the TCA cycle were significantly activated. [1]
The abstract states that cellular aging is effectively mitigated by combined regulation of metabolism, inflammation and gene expression. [1]
The source at a glance
- Study type / format
- Preclinical study reported in an abstract
- Population / context
- Aged mice and keratinocytes in the described experiments.
- Summary based on
- Study abstract
- Original publication
- October 8, 2026
Aged mice, red light and tissue H3K9ac
The abstract starts from the idea that mitochondrial metabolic activity declines with age and that altered histone acetylation contributes to senescent tissue phenotypes. In aged mice, periodic exposure to red light was reported to significantly increase acetylation of histone H3 at lysine 9 (H3K9ac) in tissues and organs. This is a measurement in mouse tissue, not a human outcome.
Supporting source [1]
SIRT4 drop and fatty acid metabolism in keratinocytes
After red light exposure, SIRT4 protein levels in keratinocytes were notably reduced, while glycolysis, fatty acid metabolism and the tricarboxylic acid (TCA) cycle were significantly activated there. Lower mitochondrial SIRT4 was linked to increased acetylation of mitochondrial metabolic proteins, especially malonyl-CoA decarboxylase, an inhibitor of carnitine palmitoyltransferase 1A (CPT1A), a rate-limiting enzyme in fatty acid oxidation. The abstract also describes SIRT1 activation via feedback, relieving inhibition of PPAR-α and activating lipid-metabolism genes.
Supporting source [1]
Acetyl-CoA, H3K9ac and senescence-related genes
According to the abstract, this lipid-metabolism activation ultimately promotes acetyl-CoA accumulation in keratinocytes, raises H3K9ac and reshapes expression of senescence-related genes. Cellular aging is then described as effectively mitigated through combined regulation of metabolism, inflammation and gene expression. These are mechanistic and cellular statements from an abstract; they do not show that red light extends lifespan or benefits human aging.
Supporting source [1]
How to interpret this
Only the abstract was reviewed; the full text was not reviewed. The work is in mice and keratinocytes, and the abstract does not report sample sizes, follow-up, lifespan or human outcomes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Deng F, Yang R, Niu J, Wang M, Liu Y, Li X, Gao Z, Yang L, Liu H, Yang Y, Yu Z, Zhang L. · europepmc.org · October 8, 2026