Re-Visiting a Post by Lou Pagnucco

[James]

> A weaker link in Lou's idea is the question of whether these senescent
> fibroblasts are responsible for lax skin etc.  It is unclear whether
> the overproduction of collagenase would have these effects, since they
> are normally ascribed to the disorderly crosslinking of OLD collagen.
> Most such collagen should be no less degradable by collagenase than
> undamaged collagen, so this overproduction may, if anything, actually
> RETARD these features of aging of skin.

I would agree with this 100% - if collagenase were the only
factor.  But I don't think lax skin has much to do with collagen
crosslinking (other than some decreased elasticity).  I think
loss of subcutaneous fat is the culprit here.  I don't know why
that happens - is it a general hormonal change, or something to
do with fibroblasts?