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
The role of metformin and its downstream targets in IgA nephropathy (IgAN) remains unclear. In this study, we used Mendelian randomization to explore potential causal links between genetic proxies of metformin targets, plasma proteins, and the risk of IgAN. Data on plasma protein, metformin target genes, and IgAN data were obtained from the IEU OpenGWAS Project. Single-nucleotide polymorphisms (SNPs) associated with metformin target genes and plasma proteins were selected as instrumental variables. We applied a two-sample and two-step Mendelian randomization approach to examine the causal relationships among these variables. Inverse variance weighted analysis revealed that electron transport flavoprotein dehydrogenase (ETFDH) inhibitors were associated with a reduced risk of IgAN (odds ratio [OR] = 0.948, 95% confidence interval [CI]: 0.923-0.973, <i>p</i> < 0.001). A significant causal relationship was identified between ETFDH inhibitors and 592 plasma proteins. Among these, 420 were identified as protective factors. Additionally, 133 plasma proteins were significantly associated with IgAN, of which 78 were identified as risk factors for IgAN. Synaptosome-associated protein 29 was identified as a plasma risk factor for IgAN (OR = 1.118, 95% CI: 1.025-1.218, <i>p</i> = 0.012) and negatively correlated with ETFDH inhibitor use (OR = 0.775; 95% CI, 0.709-0.848; <i>p</i> < 0.001). This protein appeared to mediate the effects of ETFDH inhibitors on the risk of IgAN (total effect: 0.054; mediation ratio: 52.524%). ETFDH may serve as a potential novel target downstream of metformin-associated metabolic pathways.
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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