I wanted to share an article about fibrosis. Which some people here have, and some people implies that the shrinkage etc. is just a bloodflow issue due to their experiences. And how we can increase NO- cGMP anyway?
Correcting, at least partially, the relative loss of SMCs occurring with ageing, diabetes, or cavernous nerve damage should be the target of therapy to prevent the ED associated with these conditions. Up-regulation of NO-cGMP pathway might have a role in preventing and reversing fibrosis in the tunica albuginea and in the corpora cavernosa. Therefore, long-term and continuous treatment with available PDE5-Is might be pharmacologically effective for partly reversing the underlying alterations in the corpora that lead to ED, thus potentially curing this disorder, as opposed to the current on-demand administration of these compounds for eliciting an erection. This chronic use of PDE5-Is could prevent or reverse endothelial dysfunction and possibly inhibit the atherosclerotic process. Furthermore, therapies aimed at blocking the TGF-β signalling pathway might be effective in ameliorating or preventing tunical fibrosis. This might open the door for the emergence of treatment for PD.