SRSF1 protein gave cells a younger profile and made mice less frail
A Nature Aging study from George Church's lab at Harvard identified the SRSF1 protein as a regulator of aging. In old mice, it reduced frailty progression by 44%.
Source: Transcriptomic reprogramming screen identifies SRSF1 as a regulator of aging (nature.com). Summary written with AI from the source and reviewed by rules; read the original.
What the research shows
The researchers built an age gauge based on the genes active in human skin cells and tested dozens of genes to see which made that profile younger. SRSF1, which takes part in RNA processing, did so without the cells losing their identity, and reduced markers of senescence, stress and inflammation.
In old mice, activating SRSF1 reduced frailty progression by 44% and was associated with a 14% longer median lifespan, in groups of 9 to 10 animals.
What it means
The result points to an alternative to reprogramming with Yamanaka factors, which carries toxicity risks. SRSF1 becomes a target for research into therapies for age-related diseases.
How to read it with care
The animal tests used few mice, and nothing has been tested in people. Several authors, including George Church, hold a patent on using SRSF1 and equity in a company developing therapies in this area.
This article explains research and does not replace a consultation. Anyone thinking about changing exercise, diet, supplements or treatment should talk to a doctor or another qualified health professional.