Originally Posted by Sigmoid
In Peyronie’s disease, which may or may not be similar to the the plateau, aberrant fibrin deposition is detected most of the time in histological samples.Fibrin is a blood clotting factor, it is normally dissolved by pre-embedded plasminogen (when activated it is called plasmin), however it can be prolonged in the presence of plasminogen activator inhibitor and it can bind to collagen via factor XIII. You can think of fibrin as temporary collagen.
Factor XIII is a crosslinker, it connects two pieces of connective tissue, like fibrin and fibrin to each other in a new way not part of the self assembly mechanism or fibrin to collagen.
Factor XIII, fibrin and collagen - PubMed
Factor XIII itself might play a role in the hypothetical changes to the collagen of the plateaued penis via its cross-linking abilities.
What if in the case of the plateau, chronic PE causes fibrin to bind to collagen, reinforcing it in a shortened state negating gains, and an upregulation of plasminogen activator inhibitor makes the normally temporary clotting structure semi permanent?
What do you guys think?
There’s a whole range of ideas thundersplace hasn’t explored yet, real nitty gritty aspects of connective tissue. I’m trying to gradually roll out these new subjects, past experience tells me unloading too much information at once causes aversion since people feel overwhelmed. I figure the more people know about the ins and outs of the tissues of the penis, the faster we can sort out a safe way to defeat the plateau phenomenon.
Correct me if I’m wrong but are you saying having factor eight deficiency can promote plastic deformation? If so, how can we support this idea with science and test it?
