The study’s authors pointed out that, with age, neural stem cells lose their ability to actively reproduce, leading to a decrease in neurogenesis and a gradual deterioration in cognitive functions, but they discovered a new mechanism for cell rejuvenation that relies on the DMTF1 protein, a transcription factor whose levels decrease with shortened cellular telomeres and cellular DNA damage associated with aging.
Scientists found that artificially increasing levels of DMTF1 protein in the body restored cell division and helped reduce the effects of shortened telomeres, which are responsible for cell aging.
The researchers explained that the DMTF1 protein works to regulate the Arid2 and Ss18 genes, which are components of the SWI/SNF chromatin remodeling complexes. Through these mechanisms, the DMTF1 protein maintains the activity of genes that control the cell life cycle. When DMTF1 levels decrease, these epigenetic mechanisms are disrupted, and the cells enter a state of quiescence or die. Restoring protein expression has led to the restoration of cell activity.
The aforementioned experiments were conducted on laboratory mice, so the study authors indicated that it is not yet clear whether activation of DMTF1 is safe for human use, as excessive stimulation of cell division may be associated with cancer risks.
date:2026-02-15 07:07:00
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