Using an epigenetic clock to distinguish cellular aging from senescence

The 2016 UK/UCLA human study found:

“Induction of replicative senescence (RS) and oncogene-induced senescence (OIS) are accompanied by ageing of the cell. However, senescence induced by DNA damage is not, even though RS and OIS activate the cellular DNA damage response pathway, highlighting the independence of senescence from cellular ageing.

We used primary endothelial cells (ECs) that were derived from the human coronary artery of a 19 year old male.

The fact that maintenance of telomere length by telomerase did not prevent cellular ageing defines the singular role of telomeres as that of a means by which cells restrict their proliferation to a certain number; which was the function originally ascribed to it. Cellular ageing on the other hand proceeds regardless of telomere length.

Collectively, our results reveal that cellular ageing is distinct from cellular senescence and independent of DNA damage response and telomere length.”

The following was the closest the study came to a Limitations statement:

“Although the characteristics of cellular ageing are still not well known, the remarkable precision with which the epigenetic clock can measure it and correlate it to biological ageing remove any doubt of its existence, distinctiveness and importance. This inevitably raises the question of what is the nature of this cellular ageing, and what are its eventual physical consequences.

Admittedly, the observations above do not purport to provide the answer, but they have however, cleared the path to its discovery by unshackling cellular ageing from senescence, telomeres and DNA damage response, hence inviting fresh perspectives into its possible mechanism.”

The epigenetic clock method was the same used by:

http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=7383&path[]=21162 “Epigenetic clock analyses of cellular senescence and ageing”

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