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
Cartilage metabolism balance chaos is crucial in the development and progression of osteoarthritis (OA), with chronic low-grade inflammation being the primary factor that leads to chondrocyte metabolic dysregulation. Fexofenadine (FFD) is a widely used commercially available anti-allergy compound, which has been shown to reduce inflammation. The present study finds FFD's therapeutic effects in primary human ex-vivo cultures and surgically induced murine models. Mechanism study illustrates FFD exhibits chondroprotective effect through anti-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated inflammation and pro-Transforming Growth Factor Beta (TGFβ)-associated anabolism. Specifically, FFD directly binds to cytosolic phospholipase A2 (cPLA2), down-regulating downstream NF-κB activation, resulting in alleviated catabolism. Notably, Signal Transducer and Activator of Transcription 1 (STAT1) is first identified as FFD's target by Drug affinity responsive target stability which shows the Gln-314 site is required. FFD blocks STAT1 binds to TGF-β type I receptor, leading to secondary SMAD Family Member 2 (Smad2) phorsphorylation, slightly enhances chondrocyte proliferation and matrix production. Importantly, further study demonstrates FFD directly binds Smad2 by the target proteins fishing technique, remarkably active TGFβ-related biological process. These findings provide new insights into the chondroprotective role of FFD with novel target and downstream pathway, offering promising avenues for the treatment of OA. Mechanism of Fexofenadine in treating osteoarthritis. Created with BioRender.com.
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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