An important part of PD (Peyronie’s disease) pathogenesis is the myofibroblast transformation. PDE5is (the Phosphodiesterase type-5 inhibitor) and SERMs (selective estrogen receptor modulator) help avoid fibrosis formation in vivo and in vitro PD models. This study aims to understand the effect of SERMs and PDE5is on reversing the transformation and determine the no-return point.
In-cell enzyme-linked immunosorbent assay was isolated from TA patients who underwent PD surgery. The secondary assays for this study are collagen contraction and extracellular matrix production assay. The in-cell enzyme linked type was utilized to calculate the drug target expression. SERMs and PDE5is were applied after TGF- β1, at various points
Vardenafil (PDE5i) and Tamoxifen (SERM) did not reverse the transformation in the extracellular matrix or alpha-smooth muscle actin. However, Tamoxifen reduced the collagen contraction 72 hours from the treatment. Estrogen receptor and PD5A got downregulated at 72 hours. The study was not able to quantify the estrogen receptor-α protein. After 36 hours from treatment, the peroxisome proliferator activated receptor gamma, TGFB receptor III, and antifibrotic signaling pathway got downregulated, unlike the profibrotic thrombospondin-1, which got upregulated.
The study showed the SERM and PDE5is are effective in early-phase PD. However, an in-depth study is required to test the drugs at later stages of PD.