Lou Pagnucco wrote:
> the Milan group (I cannot remember the authors) that published
> in Nature some months ago, seemed to show that mice genetically
> modified to exhibit lower rates of apoptosis lived about 35% longer.
Miglaccio et al, Nature 402(6759):309-313. True, but it is crucial
to remember that the reduction of apoptosis was not indiscriminate:
it was specifically a reduction in oxidative stress-induced apoptosis
due to knockout of one isoform of a protein. However, I still agree
strongly with you that more experiments are needed.
> Could failed, transient, apoptotic episodes result in extensive
> cell/tissue damage instead of cell death? ... Is it also possible
> that these failed cellular suicide attempts are due to mitochodrial
> oxidative bursts that manage to leave behind the biomarkers of cellular
> ageing? i.e., Is it possible that normal mitochondrial respiration has
> gotten a "bum rap" and unfairly indicted for the cellular "damage" seen
> in senescent cells? (whereas these intentional but abortive suicide
> attempts are actually responsible?)
I don't think this is very likely. We must ask what initiated the
failed apoptosis in the first place: something must have been pretty
wrong with the cell or it would not have begun the program.
Aubrey de Grey
