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FoxM1 Protein Study
Researchers at Kyoto University compared two studies on the FoxM1 protein, which regulates cell division and DNA repair programs. In one study, FoxM1 was briefly activated in young mice, while in the other, it was suppressed in very old mice, removing some senescent cells. The authors linked the difference to age, organ, and cell type.
The review, published on August 17, compared these results, noting that senescent cells stop dividing but remain in tissue, releasing inflammatory signals. FoxM1 may support their survival, and when briefly activated from a young age, tissue restoration programs. In a 2022 study, researchers activated an added active version of FoxM1 in mice from eight weeks of age: three days of work, four days of pause, for a total of 80 weeks.
The authors reported that in progeroid and naturally aging animals, age-related signs weakened, and lifespan increased. In a 2025 article, the authors investigated the link between PGAM1 and Chk1 in senescent cells, finding that their interaction stabilized HIF-2α, a regulator of glucose metabolism genes, and increased FoxM1 activity. The cell received material for nucleotide synthesis, the building blocks of DNA, and maintained a survival program, as described in the Nature Aging, July 2026.
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