
Stem cell competition orchestrates skin homeostasis and ageing - evo_9
https://www.nature.com/articles/s41586-019-1085-7
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sagebird
I hope you will not take this as me encouraging a conspiracy theory —

I sometimes wonder what would happen if someone stumbled upon a simple, robust
and general method for halting aging using the likes of stem cells. Ordinarily
this sort of discovery happens in plain sight— over many years of acedemic
research, published papers, animal studies and human studies. But suppose it
occurred in a private lab and was kept, basically, secret. I could imagine a
government being hesitant to release this info if they thought lay people
could implement t the treatment themselves and live multi thousands of years.

But I also suspect that a few rich and powerful people would want to have a
go. It would be interesting to see how they conceal the fact— do they fake
death multiple times? Even if a government is able to restrict interested
billionaires and powerful people from participating, they may feel a need to
keep a population of long span humans— as a competitive hedge against other
nations’ possible participation. It’s possible that this is happening now,
though I know of absolutely no evidence of that.

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blockmarker
I don't believe that will happen, because that treatment would massively boost
the economy. Nowadays we have to spend around 23 years until a person can be
productive, then they have to learn to be more efficient, and in a few years
they have children and focus less on their job. As well as they becoming
older, losing efficiency until they retire and then they consume the resources
of social security for twenty or more years.

Eternal youth would be so good to the economy that it would never be hidden.

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pmarreck
Any word on what can stimulate production of COL17A1, or is it still too new a
research area?

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medymed
From the paper:

"We identified two chemicals—Y27632 and apocynin—that induced COL17A1
expression in keratinocytes. To test whether these compounds increased the
self-renewing capabilities of epidermal stem cells in vitro, we performed
colony-formation assays40,41; Y-27632 increased colony number, and both drugs
increased colony size (Extended Data Fig. 9m–p). Application of these drugs to
full-thickness skin wounds significantly promoted wound repair, similarly to
the effect of overexpression of human COL17A1 in mice (Extended Data Fig.
9q–s). Collectively, these data show that COL17A1-inducing drugs promote skin
wound healing through re-epithelization of the wound edge with epidermal stem
cell expansion, and point towards directions for facilitating skin
regeneration and reducing skin ageing."

It seems like one very promising application could be in promoting wound
healing in certain populations e.g. venous stasis ulcers, pressure ulcers, and
many other chronic wounds that don't heal well especially in the elderly (if
the treatment were safe). That would be fantastic.

But the use of the term anti-aging effects in this paper is suspect. COL17A is
part of the basement membrane holding together the thin epidermis and thicker
underlying dermis, whereas much aging related research that focuses on
'collagen' loss relates to the amount of collagen I in the thicker underlying
dermis. Loss of dermal collagen I with aging is associated with cosmetic
changes like thin skin (dermal thinning) and wrinkling.

It would be surprising if increased expression of COL17A1 at the basement
membrane dramatically induced cosmetic anti-aging effects in the sense of
increased level of collagen I in the dermis. Also, it may be a band-aid for
one particular cellular function that is important for local tissue structure
and cell functions, but the underlying causes of general aging change in cells
(mutation accumulation, UV damage, oxidative damage, etc) probably are not
being addressed or reversed.

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ilaksh
I really doubt its just this one thing that is responsible for aging even just
for skin.

I subscribe to the SENS theory of aging (sens.org).

