《細胞》：基因技術逆轉衰老並延長壽命

Salk 研究院的科學家們通過在體細胞中周期性表達一組在胚胎早期活躍的基因（山中分子，Yamanaka factors），減緩了小鼠衰老相關癥狀並延長壽命達30%。

Ocampo等人文章的摘要

衰老是人類眾多疾病的主要風險因素。體外研究表明將細胞重編程為多功能細胞可逆轉細胞年齡，但是尚未在體內研究中得到證實。在此我們報告通過短期周期性表達 Oct4, Sox2, Klf4, 和 c-Myc (OSKM) 部分重編程細胞可在一個小鼠早衰模型中改善與衰老相關的細胞及生理癥狀。與此類似，在年老的正常小鼠體內表達 OSKM 幫助改善代謝癥狀和肌肉損傷。這一表觀遺傳重編程對衰老相關癥狀的改善指向哺乳動物衰老中表觀遺傳失調的驅動作用。建立活體動物中調控衰老相關表觀遺傳表徵的平台可能提供對衰老生理基礎的更深認識。

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 mouse model 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.

可以為人類續命嗎？

作者表示，距離開始人類臨床試驗可能需要10年時間 [2]。

[1] Ocampo, A., Reddy, P., Martinez-Redondo, P., Platero-Luengo, A., Hatanaka, F., Hishida, T., … Izpisua Belmonte, J. C. (2016). In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming. Cell, 167(7), 1719–1733.e12. http://doi.org/10.1016/j.cell.2016.11.052 （開放訪問）

[2] Turning back time: Salk scientists reverse signs of aging - Salk Institute for Biological Studies

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