Discussion in 'Hair Loss and Alopecia Published Studies' started by InBeforeTheCure, Dec 29, 2017.
Minoxidil Induction of VEGF Is Mediated by Inhibition of HIF-Prolyl Hydroxylase
Interesting, thank you for the post.
Would you say this is a significant reason for minoxidil working?
I've seen some other articles on what minoxidil does, so I'm wondering whether it might be downstream of inhibiting PHD-2
Can we find other PHD-2 inhibitors maybe without the side effects of minoxidil?
Not to derail, but I've seen you've posted on genetic expression in Androgenetic Alopecia.
ARNTL2 is 12x downregulated compared to non-balding. One of the most Downregulated in a particular study.
HIF-1alpha dimerizes with ARNTL(NOT arntl2, but they are parralelogs according to wiki) to induce VEGF expression
According to this, suggested, aryl hydrocarbon receptor AhR overactivity robs HIF-1alpha from its partner ARNT.
Is it possible there is some AhR overactivity and the body is downregulating ARNT2 to limit it, I'm interested in your take of what other genes AhR might be related to in terms of balding.
Re: Would you say this is a significant reason for minoxidil working?
Probably not, actually.
From the paper:
Since minoxidil sulfate (which opens potassium channels) is the metabolite responsible for hair growth, and other potassium channel openers like diazoxide also stimulate hair growth, this mechanism probably doesn't contribute much.
There's a contradictory result (there often are) from another microarray dataset where median expression of ARNTL2 is higher in bald scalp, but with wildly varying values for each person. ARNTL2 is one of the circadian clock genes, also involved in hair cycling (here is a study if you're interested). Maybe there's some crosstalk between the clock genes and HIF-1 in the hair cycle as well?