How hair is formed (the end of catagen and early anagen)

I was digging into the reasons why even castration doesnt grow the vellous hair back. And I think i kinda understand it now.

We know that sulfasalazine and benoxaprofen guys experienced reversak of mpb from slick bald head to full coverage and original density.

in other words, it seems likely that their vellous tiny hair cycled rapidly from miniaturised vellous follicle to full healthy follicle.

The purpose of this thread is to figure out and find evidence of how this happens. How new follicle is formed at the end of catagen and begining of new anagen.

Im hypothetising that this is when their reversal happened.

So here we are. Our problem is that we have vellous follicles where hair bulge and hair germ cells are reduced.

Using cell samples
from bald and non-bald scalp from AGA individuals
and three-color flow cytometry analysis,
the investigators found that slow cycling stem
cell predecessors rich in cytokeratin 15 (K15)
were maintained in bald scalp samples, but K15
dim, CD200, integrin a6 and CD34 bright cells localized to the
lower bulge, and hair germ (HG) cells were dramatically depleted
in bald scalp.

And these two are probably what creates the anagen follicle:

Hair follicles (HFs) undergo cyclic bouts of degeneration, rest, and regeneration. During rest (telogen), the hair germ (HG) appears as a small cell cluster between the slow-cycling bulge and dermal papilla (DP). Here we show that HG cells are derived from bulge stem cells (SCs) but become responsive quicker to DP-promoting signals. In vitro, HG cells also proliferate sooner but display shorter-lived potential than bulge cells. Molecularly, they more closely resemble activated bulge rather than transit-amplifying (matrix) cells. Transcriptional profiling reveals precocious activity of both HG and DP in late telogen, accompanied by Wnt signaling in HG and elevated FGFs and BMP inhibitors in DP. FGFs and BMP inhibitors participate with Wnts in exerting selective and potent stimuli to the HG both in vivo and in vitro. Our findings suggest a model where HG cells fuel initial steps in hair regeneration, while the bulge is the engine maintaining the process.

and why lattice will be most probably the same. And why mice models are useless.

to counteract this one would need to find a way how to turn the stem cells into the missing hair bulb and hair germ progenitor cells