Figure 5.

Schematic representation of the molecular mechanism underlying BEC proliferation in BPH. Activation of the cGMP/PKG signaling pathway in CD8⁺ T cells decreased NF‐κB phosphorylation and CCL5 secretion, resulting in the inhibition of CCL5/STAT5/CCND1 signaling in BECs and decrease of their proliferation in low androgen conditions. BEC, BPH epithelial cell; BPH, benign prostatic hyperplasia; cGMP, cyclic guanosine monophosphate; NF‐κB, nuclear factor‐κB; PDE5, phosphodiesterase type 5; PDE5‐I, PDE5 inhibitors; PKG, protein kinase G; STAT5, signal transducer and activator of transcription 5 [Color figure can be viewed at wileyonlinelibrary.com]