Toward a unified theory of aging and regeneration

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 re...

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Bibliographic Details
Published in:Regenerative medicine 2019-09, Vol.14 (9), p.867-886
Main Authors: West, Michael D, Sternberg, Hal, Labat, Ivan, Janus, Jeffrey, Chapman, Karen B, Malik, Nafees N, de Grey, Aubrey Dnj, Larocca, Dana
Format: Article
Language:English
Subjects:
acetyl-CoA
Age
Aging
AMPK
Cancer
Cardiovascular disease
Cell division
dietary restriction
DNA methylation
Epigenetics
Gene expression
Genomes
Humans
Hypotheses
Mammals
Models, Biological
Mortality
mTOR
Neoplasms - metabolism
Neoplasms - pathology
Neoplasms - therapy
Organisms
pluripotent stem cells
Regeneration
Twins
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Summary: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.
ISSN:1746-0751
1746-076X
DOI:10.2217/rme-2019-0062