allora ho letto il link messo da foxtrot e nonostante l'inglese per me non sia un problema devo dire che è un casino tradurlo a causa dei 3000 termini più o meno tecnici usati...
i passaggi interessanti credo siano questi comunque:
PGD2 is formed by the following sequence of enzyme reactions after cell activation 1) cytosolic phospholipase A2 is translocated to the endoplasmic reticulum and perinuclear membranes in a Ca2+-dependent manner, where it cleaves arachidonic acid from the membrane phospholipids; 2) arachidonic acid is converted to PGH2, a common precursor of various prostanoids, by the membrane-bound cyclooxygenases (COXs); and 3) PGH2 is further isomerized to PGD2 by PGD synthase (PGDS) (source vinman)
PGD2 upregulates p53 which causes Endothelial Cell Apoptosis (anti angiogenesis), p53 induces dkk1, dkk1 --> Result == Anti angiogenesis + apoptosis (with otuer words catagen + apoptosis == HAIRLOSS! <--pgd2 induces Caspase 3 which leads to pkc-> apoptosis -> Lpgds, bdnf.... its w whole loop back chain reaction.
15-Deoxy- (12,14)-prostaglandin J2 (15-dPGJ2)Induces Vascular
Endothelial Cell Apoptosis through the Sequential Activation
of MAPKS and p53
http://www.jbc.org/content/283/44/30273.full.pdf
now p53 in aga.
The frontal bald area of patients showed significantly higher levels of X-ray Cross Complementing-1 (XRCC1; P<0.001) and p53 (P<0.001) expression when compared with occipital hairy area of patients and frontal area of controls
http://www.ncbi.nlm.nih.gov/pubmed/18702626
so wtf p53 role with dkk1?
Dickkopf-1, an inhibitor of the Wnt signaling pathway, is induced by p53
http://www.nature.com/onc/jour...14/full/1203503a.html
You know the role of igf in aga, we know that some people taking finasteride and respond well have increased levels of igf.
Here for example http://www.alopezie.de/diskuss...upregulated_igf-1.pdf
also http://www.ncbi.nlm.nih.gov/pubmed/22363152
So there is a relationship with dht and igf...
See what's behind this
The prostaglandins (in order of potency) PGJ2 > PGA1 > PGA2 all significantly repressed IGF-I gene expression
http://www.ncbi.nlm.nih.gov/pubmed/9545524
The 15d-PGJ2 is Cyclopentenone prostaglandin...
Are you starting to see the puzzle in AGA?.....
Hey i can see the aga image in the puzzle!!! I believe for the full 100% in this approach and I know this is It with full confidence!.
Yes off course the wnt pathway can be activated/inhibited by so many genes and most info on the net supports it TNF-a for example->dkk1...., this is most likely the It, with hard evidence. also we DO know,aswell, that its known pgd2 exhibits pge2s (lost the source its somewhere here on forum).
All by all, if we can create the original growth environment, (normal PGD2 signaling), will lead to at least stabilization (which is currently the case on most users), but in long term, the damage of all years Anti angiogenesis and apoptosis effect of PGD2, could be reversed. But off course it will take time. We can help speeding up this process, by adding exogenous PGe2, using things like tb4, minox, vpa, Hif1 inducers. This is how I see it and Im 100% confident about it. take some DAYS to read everything over and over, before replaying.
nella parte finale l'utente ammette che non si sa ancora bene quale sia la causa scatenante dell'AGA giovanile ed ipotizza una serie di cose tipo l'ambiente nel quale viviamo, il cibo (in particolare una proteina specifica se ho ben capito) e mutazioni dei geni.