Harvard Medical School researchers led by George M. Church reported on the 14th in Nature Aging that an AI-assisted search identified SRSF1, a gene that extended median lifespan by 14% and slowed frailty progression by 44% in aged mice. The team said SRSF1 reactivated DNA repair programs in aged cells while reducing three aging markers: damaged cells that persist and release inflammatory substances, stress from misfolded proteins, and chronic inflammation. The experiments used cultured human cells and mice; human treatment is not yet feasible.

The researchers trained an age-prediction model on gene-expression data from 464 human skin fibroblast samples across age groups. The machine-learning model estimated “transcriptomic age,” a measure based on gene activity. They screened candidate genes for overexpression that could lower that estimated age in senescent fibroblasts, and SRSF1 showed the strongest predicted rejuvenation effect. The study involved an international collaboration that included Alexandru Plesa of the Wyss Institute.

The team said SRSF1 acts as an RNA-splicing factor, joining selected segments of messenger RNA so cells can produce proteins needed for repair and maintaining vitality. In the experiments, treated cells retained their original shape and function, and researchers did not observe increased cancer risk. The authors contrasted this with Shinya Yamanaka’s cellular reprogramming approach, which turns mature cells into induced pluripotent stem cells but can erase their original identity and raise cancer risk.

For the mouse experiments, researchers packaged SRSF1 in a liver-targeting adeno-associated virus and administered it to aged mice. Although delivery was focused mainly on the liver, the team reported effects across the body: frailty progression was 44% slower than in controls, and median survival was extended by 14%. They hypothesized that changes in liver tissue may have affected aging in other organs. The research team said it would continue developing ways to deliver SRSF1 safely to organs and tissues for possible clinical use.

The findings remain an early-stage result from human cell cultures and mice. Applying them to people will require technology to deliver the gene safely to target tissues and control its activation level. Researchers said the long-term safety of adeno-associated virus vectors and possible side effects from excess SRSF1 activity require further study. The article also says machine-learning screening has widened the search for genes linked to aging, but reports no human trial or clinical application.

Harvard Medical School researchers led by George M. Church reported on the 14th in Nature Aging that an AI-assisted search identified SRSF1, a gene that extended median lifespan by 14% and slowed frailty progression by 44% in aged mice. The team said SRSF1 reactivated DNA repair programs in aged cells while reducing three aging markers: damaged cells that persist and release inflammatory substances, stress from misfolded proteins, and chronic inflammation. The experiments used cultured human cells and mice; human treatment is not yet feasible.

The researchers trained an age-prediction model on gene-expression data from 464 human skin fibroblast samples across age groups. The machine-learning model estimated “transcriptomic age,” a measure based on gene activity. They screened candidate genes for overexpression that could lower that estimated age in senescent fibroblasts, and SRSF1 showed the strongest predicted rejuvenation effect. The study involved an international collaboration that included Alexandru Plesa of the Wyss Institute.

The team said SRSF1 acts as an RNA-splicing factor, joining selected segments of messenger RNA so cells can produce proteins needed for repair and maintaining vitality. In the experiments, treated cells retained their original shape and function, and researchers did not observe increased cancer risk. The authors contrasted this with Shinya Yamanaka’s cellular reprogramming approach, which turns mature cells into induced pluripotent stem cells but can erase their original identity and raise cancer risk.

For the mouse experiments, researchers packaged SRSF1 in a liver-targeting adeno-associated virus and administered it to aged mice. Although delivery was focused mainly on the liver, the team reported effects across the body: frailty progression was 44% slower than in controls, and median survival was extended by 14%. They hypothesized that changes in liver tissue may have affected aging in other organs. The research team said it would continue developing ways to deliver SRSF1 safely to organs and tissues for possible clinical use.

The findings remain an early-stage result from human cell cultures and mice. Applying them to people will require technology to deliver the gene safely to target tissues and control its activation level. Researchers said the long-term safety of adeno-associated virus vectors and possible side effects from excess SRSF1 activity require further study. The article also says machine-learning screening has widened the search for genes linked to aging, but reports no human trial or clinical application.