{Reference Type}: Journal Article
{Title}: Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia.
{Author}: Li T;Zhang Y;Zhou Z;Guan L;Zhang Y;Zhou Z;Wang W;Zhou X;Cui D;Jiang C;Ruan Y;
{Journal}: Biol Direct
{Volume}: 19
{Issue}: 1
{Year}: 2024 Aug 2
{Factor}: 7.173
{DOI}: 10.1186/s13062-024-00504-y
{Abstract}: Myofibroblast buildup and prostatic fibrosis play a crucial role in the development of benign prostatic hyperplasia (BPH). Treatments specifically targeting myofibroblasts could be a promising approach for treating BPH. Tadalafil, a phosphodiesterase type 5 (PDE5) inhibitor, holds the potential to intervene in this biological process. This study employs prostatic stromal fibroblasts to induce myofibroblast differentiation through TGFβ1 stimulation. As a result, tadalafil significantly inhibited prostatic stromal fibroblast proliferation and fibrosis process, compared to the control group. Furthermore, our transcriptome sequencing results revealed that tadalafil inhibited FGF9 secretion and simultaneously improved miR-3126-3p expression via TGFβ1 suppression. Overall, TGFβ1 can trigger pro-fibrotic signaling through miR-3126-3p in the prostatic stroma, and the use of tadalafil can inhibit this process.