This shows that SHH has significant potential for development as a therapy for morphological and physiological changes in the penis that cause ED.
The reversibility of SHH inhibition has wide implications. Mutations in the Shh signaling pathway that target Ptchl, Smo, and Glil are associated with certain forms of cancer, including prostate, skin, and esophageal.
These mutations cause continuous transcription of Shh targets and are not caused by an overabundance of Shh itself. The SHH inhibitor cyclop-amine is currently being tested to fight tumor growth. If given systemically, this inhibitor will likely alter normal penile morphology and the architecture of other organs where Shh remains active in the adult. Penile remodeling occurs quickly after SHH inhibition and is extensive after 7 days. The morphological changes caused by SHH inhibition in the penis are reversible, at least after short-term inhibition (<14 days). This suggests that SHH inhibitors given to prostate cancer patients will modify normal penile morphology and cause ED. However this process may be reversible once SHH inhibition is removed.