Fig. 2

Age reprogramming in vivo. Schematic depiction of the experiment by Ocampo et al. [28]. Top row: Short-term or cyclic (2 days “on” and 5 days “off”) expression of OSKM reprogramming factors in fibroblasts from LAKI progeria mice (blue) lead to age reprogramming of epigenetic rejuvenation, DNA damage, senescence, mitochondrial dysfunction and stress response. The first four characteristics are known hallmarks of ageing [9]. Age-reprogrammed fibroblast from the LAKI progeria mouse is given in red. Similar results were obtained with old wild-type murine and human fibroblasts. Middle row: Cyclic expression of OSKM reprogramming factors in LAKI progeria mouse leads to age reprogramming of DNA damage, senescence, stress response and epigenetic rejuvenation. The mice also exhibit enhanced regeneration of satellite cells in the muscle after chemical injury. They also have increased median and maximal lifespan. Bottom row: Cyclic expression of OSKM reprogramming factors in 12-month-old wild-type mice promotes regeneration of β cells in the pancreas and satellite cells of the muscle after chemical injury. Other parameters were not tested and are given as a question mark. An upward facing arrow depicts an increase in a particular characteristic after cyclic OSKM expression and the downward arrow a decrease