1. Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia.
- Author
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Li T, Zhang Y, Zhou Z, Guan L, Zhang Y, Zhou Z, Wang W, Zhou X, Cui D, Jiang C, and Ruan Y
- Subjects
- Male, Humans, Prostate drug effects, Prostate metabolism, Myofibroblasts metabolism, Myofibroblasts drug effects, Transforming Growth Factor beta1 metabolism, Transforming Growth Factor beta1 genetics, Cell Proliferation drug effects, Prostatic Hyperplasia metabolism, Prostatic Hyperplasia drug therapy, Prostatic Hyperplasia genetics, MicroRNAs genetics, MicroRNAs metabolism, Tadalafil pharmacology, Phosphodiesterase 5 Inhibitors pharmacology, Fibrosis, Fibroblast Growth Factor 9 metabolism, Fibroblast Growth Factor 9 genetics
- 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., (© 2024. The Author(s).)
- Published
- 2024
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