https://www.nature.com/articles/s41586-020-2975-4 > Ageing is a degenerative process that leads to tissue dysfunction and death. > A proposed cause of ageing is the accumulation of epigenetic noise that > disrupts gene expression patterns, leading to decreases in tissue function > and regenerative capacity1,2,3. Changes to DNA methylation patterns over time > form the basis of ageing clocks4, but whether older individuals retain the > information needed to restore these patterns—and, if so, whether this could > improve tissue function—is not known. Over time, the central nervous system > (CNS) loses function and regenerative capacity5,6,7. Using the eye as a model > CNS tissue, here we show that ectopic expression of Oct4 (also known as > Pou5f1), Sox2 and Klf4 genes (OSK) in mouse retinal ganglion cells restores > youthful DNA methylation patterns and transcriptomes, promotes axon > regeneration after injury, and reverses vision loss in a mouse model of > glaucoma and in aged mice. The beneficial effects of OSK-induced > reprogramming in axon regeneration and vision require the DNA demethylases > TET1 and TET2. These data indicate that mammalian tissues retain a record of > youthful epigenetic information—encoded in part by DNA methylation—that can > be accessed to improve tissue function and promote regeneration in vivo.
I haven't found an open copy of that. But there is this: Reversal of ageing- and injury-induced vision loss by Tet-dependent epigenetic reprogramming https://www.biorxiv.org/content/10.1101/710210v1 -- ↙↙↙ uǝlƃ - .... . -..-. . -. -.. -..-. .. ... -..-. .... . .-. . FRIAM Applied Complexity Group listserv Zoom Fridays 9:30a-12p Mtn GMT-6 bit.ly/virtualfriam un/subscribe http://redfish.com/mailman/listinfo/friam_redfish.com archives: http://friam.471366.n2.nabble.com/ FRIAM-COMIC http://friam-comic.blogspot.com/
