| Literature DB >> 31455183 |
Michael D West1, Hal Sternberg1, Ivan Labat1, Jeffrey Janus1, Karen B Chapman2, Nafees N Malik1,3, Aubrey Dnj de Grey1,4, Dana Larocca1.
Abstract
Growing evidence supports the antagonistic pleiotropy theory of mammalian aging. Accordingly, changes in gene expression following the pluripotency transition, and subsequent transitions such as the embryonic-fetal transition, while providing tumor suppressive and antiviral survival benefits also result in a loss of regenerative potential leading to age-related fibrosis and degenerative diseases. However, reprogramming somatic cells to pluripotency demonstrates the possibility of restoring telomerase and embryonic regeneration pathways and thus reversing the age-related decline in regenerative capacity. A unified model of aging and loss of regenerative potential is emerging that may ultimately be translated into new therapeutic approaches for establishing induced tissue regeneration and modulation of the embryo-onco phenotype of cancer.Entities:
Keywords: AMPK; DNA methylation; acetyl-CoA; aging; dietary restriction; epigenetics; mTOR; pluripotent stem cells; regeneration
Mesh:
Year: 2019 PMID: 31455183 DOI: 10.2217/rme-2019-0062
Source DB: PubMed Journal: Regen Med ISSN: 1746-0751 Impact factor: 3.806