In vivo partial reprogramming alters age-associated molecular changes during physiological aging in mice.
Level 5 - mechanism / opinion, no new human data
Animal experiment without human clinical data.
PubMed 37118377 · doi:10.1038/s43587-022-00183-2
What was done
Researchers administered long-term in vivo partial reprogramming protocols using cyclic expression of the Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc) with different treatment durations and onset timings in naturally aging wild-type mice. They evaluated tissue-specific effects (including kidney and skin), organism-level outcomes, epigenetic clock reversion, and metabolic and transcriptomic changes.
What was found
The abstract reports no numerical data, sample sizes, or effect sizes. It states that long-term partial reprogramming produced rejuvenating effects across multiple tissues and at the organismal level, reversed epigenetic clock measurements, and reduced the expression of genes involved in inflammation, senescence, and cellular stress responses, with longer regimens demonstrating greater benefits than shorter ones without apparent safety failure.
Why it matters
This work shows that cyclical in vivo epigenetic reprogramming can be maintained long-term in physiologically normal aging mammals to reverse molecular hallmarks of aging, rather than just in progeroid disease models.
Limits
The study is restricted entirely to wild-type mice; translation, delivery methods, and safety in humans remain unestablished. The abstract does not provide specific sample sizes, survival or lifespan statistics, quantitative effect sizes, or detailed toxicity endpoints.
Cited by
- supports Partial cellular reprogramming in wild-type mice and in cultured cells reverses epigenetic age and improves cellular function.