A unified theory for aging and regeneration
The antagonistic pleiotropy hypothesis of mammalian ageing is gaining support. Accordingly, the changes in gene transcription following the pluripotency and subsequent transitions, such as the embryonic – fetal transitions, provide tumor suppression and antiviral benefits, but also lead to a loss in regenerative capacity, leading to age related fibrosis, and degenerative disease. Reprogramming somatic cell to pluripotency, however, shows the ability to restore telomerase pathways and embryonic regeneration and reverse the age-related decline of regenerative capability. The emergence of a unified model for aging and the loss of regenerative capacity may lead to new therapeutic approaches that can be used in the establishment of induced tissue regeneration, and modulation of embryo-onco cancer phenotype.
Keywords:
acetyl-CoA
Ageing
AMPK
Dietary restriction
DNA methylation
epigenetics
mTOR
Pluripotent stem cell
regeneration
The aging process is usually defined as the progressive degeneration of an organism with time. In the post-reproductive years, the mortality risk increases exponentially. While everyday environmental risks (e.g. stochastic risk) are necessary to increase mortality over time, these risks are not considered central to the definition for the aging process [1,2]. The gonads are a good example of this. Benjamin Gompertz, in order to distinguish aging from damage that occurs over time stochastically, described aging as an exponential process that leads to an increase in mortality. This is Rm = R0eat, where ‘Rm’ represents the probability that mortality will occur between the ages of ‘t’ to ‘t+1’.
Source:
https://www.futuremedicine.com/doi/10.2217/rme-2019-0062
