인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
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
Atrial remodelling is the principal pathological mechanism for atrial fibrillation (AF) development and progression. Long noncoding RNAs (LncRNAs) exhibit important effects on cardiovascular diseases. However, the role of LncRNAs in AF development requires further investigation. This study aimed to explore the function and mechanism of LncRNAs in AF. The differentially expressed LncRNAs of atrial tissue in a mouse AF model, which was established via continuous infusion of Ang II for 3 weeks, were screened with RNA sequencing. Experiments included an electrophysiological study; Masson, H&E and TUNEL staining; flow cytometry; and RNA pull-down; FISH and RNA immunoprecipitation assays were performed to define the function and underlying mechanisms of LncRNAs in AF susceptibility and atrial remodelling. The Kaplan-Meier method was used to plot the curve of freedom from atrial tachyarrhythmia. LncRNA Dleu2 expression was increased in atrial tissue and peripheral blood and was positively associated with left atrial fibrosis in persistent AF. Furthermore, elevated expression of LncRNA Dleu2 was correlated with a higher AF recurrence rate after ablation at the 24-month follow-up (65.0% vs. 85.0%, p = 0.03). Accordingly, upregulation and downregulation of LncRNA Dleu2 expression could regulate atrial remodelling and AF susceptibility, and we also demonstrated that LncRNA Dleu2 directly bound to Nr4a1. Subsequently, inhibition of Nr4a1 expression could also regulate AF susceptibility and atrial remodelling and reverse the effects of LncRNA Dleu2 on AF occurrence. This study demonstrated that LncRNA Dleu2 was independently associated with atrial fibrosis and AF recurrence after ablation, and contributed to AF susceptibility by directly targeting Nr4a1.
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.