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
Vascular calcification (VC) in type 2 diabetes (T2D) poses a serious threat to the life and health of patients. However, its pathogenesis remains unclear, resulting in a lack of effective treatment for the root cause. It is found that both intestinal Bacteroides fragilis (BF) and peripheral M2 monocytes/macrophages are significantly elevated in patients with T2D VC. M2 macrophages are identified as a significant risk factor for T2D VC. Both BF and their extracellular vesicles (EV) promote T2D VC and facilitate macrophage M2 polarization. Macrophages clearance significantly antagonized BF EV-induced T2D VC in mice. Mechanistically, EV-rich double-stranded DNA (dsDNA) activates stimulator of interferon response cGAMP interactor 1 (Sting), promotes myocyte enhancer factor 2D (Mef2d) phosphorylation, upregulates tribbles pseudokinase 1 (Trib1) expression, and induces macrophage M2 polarization. Concurrently, Mef2d activated by the EV targets and upregulates the expression of pro-calcification factor Serpine1, thereby exacerbating T2D VC. Clinical studies have shown that Serpine1 is significantly elevated in the peripheral blood of patients with T2D VC and is closely associated with T2D VC. In summary, this study reveals that intestinal BF promotes Trib1 expression through the EV-Sting-Mef2d pathway to induce macrophage M2 polarization and upregulates serpin family E member 1 (Serpine1) expression, thereby aggravating T2D VC. The findings provide a new theoretical and experimental bases for optimizing the strategies for prevention and treatment of T2D VC.
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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