This 2015 California rodent study found:
“A surprising beneficial effect of mitochondrial dysfunction at young age (accelerated wound closure), and a potential mechanism for the reduced epidermal regeneration at older ages (stem cell depletion).”
The researchers generated mitochondrial oxidative stress by deleting:
“A nuclear gene that encodes the mitochondrial antioxidant enzyme superoxide dismutase 2 (Sod2). Epidermal Sod2 loss induced cellular senescence, which irreversibly arrested proliferation in a fraction of keratinocytes.
Surprisingly, in young mice, Sod2 deficiency accelerated wound closure, increasing epidermal differentiation and reepithelialization, despite the reduced proliferation.
In contrast, at older ages, Sod2 deficiency delayed wound closure and reduced epidermal thickness, accompanied by epidermal stem cell exhaustion.”
The term “cellular senescence” used above is defined as: a cell can no longer replicate. Although the word “senescence” implies that chronological age is a factor, “cellular senescence” by definition isn’t about age.
In my view, this study’s etiologic findings weren’t “age” itself, but:
- Sod2 deficiency – the subjects’ genetic condition – which increased free radicals;
- The interplay of Sod2 deficiency with varying keratinocyte and epidermal stem cell levels; and
- Sod2 deficiency’s influence on other items shown in the supplementary material, to include varying “mRNA levels of wound healing-related growth factors.”
I guess the “age was the cause” meme is hard to stop repeating, though. The researchers said they could “identify a previously unidentified age-dependent role for mitochondria in quality and wound closure,” and repeated the “age-dependent” phrase in the study title.
Is pitching this meme an organizational imperative for the Buck Institute for Research on Aging, no matter what their researchers find?
http://www.pnas.org/content/112/33/10407.full “Pleiotropic age-dependent effects of mitochondrial dysfunction on epidermal stem cells”