期刊
CELL
卷 167, 期 7, 页码 1719-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.11.052
关键词
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资金
- US NIH Ruth L. Kirschstein National Research Service Award Individual Postdoctoral Fellowship
- Muscular Dystrophy Association
- Fundacion Alfonso Martin Escudero
- Hewitt Foundation
- Uehara Memorial Foundation
- Nomis Foundation
- JSPS Postdoctoral Fellowship for Research Abroad
- University of California, San Diego
- G. Harold and Leila Y. Mathers Charitable Foundation
- Leona M. and Harry B. Helmsley Charitable Trust [2012-PG-MED002]
- Moxie Foundation
- Glenn Foundation
- Universidad Catolica San Antonio de Murcia (UCAM)
- Fundacion Dr. Pedro Guillen
Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mousemodel of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.
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