인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Benign prostatic hyperplasia (BPH) is an age-related condition in men with a poorly defined etiology. Chronic inflammation is increasingly recognized as a key contributor to BPH progression; however, the underlying mechanisms remain incompletely understood. This study aimed to elucidate the role of a TNF-α-induced inflammatory microenvironment in regulating BPH progression. We demonstrated that TNF-α levels were significantly elevated in patients with BPH and positively correlated with key clinical characteristics. In vitro, TNF-α promoted the proliferation of prostatic cells. Mechanistically, TNF-α induced the overexpression of SOX4, which subsequently activated the TGF-β/Smad2/3 signaling axis, thereby enhancing cellular proliferation, promoting epithelial-mesenchymal transition (EMT), and exacerbating fibrosis. Importantly, metformin (Met) treatment reduced the expression levels of relevant inflammatory cytokines in the serum of BPH rats. Further analysis confirmed that Met inhibited the TGF-β/Smad2/3 signaling pathway by downregulating the expression of SOX4, thus suppressing cell proliferation, reversing EMT, alleviating fibrosis, and ultimately exerting anti-BPH effects. Collectively, our findings suggest that TNF-α promotes BPH progression via activation of the SOX4/TGF-β/Smad2/3 axis, while Met exerts therapeutic effects by targeting this pathway. These results highlight SOX4 as a potential therapeutic target for BPH and support the clinical potential of Met in BPH management.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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