Abstract
Previous studies have demonstrated an increased incidence of benign prostatic hyperplasia (BPH) in men with prostatitis. In addition to androgens and age, recent studies also pointed to an important role for inflammation in causing and promoting the progression of BPH. Inflammatory infiltrates are frequently observed in prostate tissue specimens, and the degree of inflammation has been correlated with prostate volume and weight. Furthermore, a pro-inflammatory microenvironment is closely related to BPH stromal hyperproliferation and tissue remodeling, although its role in BPH remains unclear. Accumulating evidence indicates that HMGB1 acts as a potent proinflammatory cytokine that contributes to the pathogenesis of many inflammatory and infectious disorders. Experimental studies also reported that HMGB1 promotes cell chemotaxis and proliferation. These observations led us to propose that HMGB1 contributes to the progress of BPH, and that targeting the HMGB1 signaling pathway might be a new strategy to treat prostatic enlargement.
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