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Fibroblast proliferation in prostatic tissue refers to the increase in number and/or activation of fibroblasts—mesenchymal cells responsible for extracellular matrix production and tissue remodeling—within the prostate gland. In benign prostatic hyperplasia and prostate cancer, proliferating fibroblasts (and their activated phenotype, "myofibroblasts") contribute to stromal expansion, fibrosis, and create a microenvironment that supports epithelial proliferation and disease progression[1][2][3][4]. This proliferation is regulated by a variety of molecular factors, including growth factors (e.g., TGF-β, FGF), inflammatory cytokines (e.g., IL-8), and changes in the tissue environment such as hypoxia[1][3]. Although drugs such as androgen deprivation therapy and TGF-β inhibitors may affect fibroblast proliferation indirectly, the process itself is not a stand-alone drug target, but rather a pathophysiological outcome of upstream molecular changes.
Related drugs generally act by suppressing androgen-mediated growth, modulating cytokine/growth factor signaling, or inhibiting specific kinases
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