Nature子刊：房颤竟是一种自身免疫疾病？

Core Viewpoint - Atrial Fibrillation (AF) is the most common persistent arrhythmia, leading to significant morbidity and mortality due to heart failure and thromboembolic strokes. There is an urgent need for better understanding of the pathways that trigger AF to develop effective and safe treatments [2]. Group 1: Research Findings - A study published by researchers from Harvard Medical School indicates that B cells promote atrial fibrillation through the production of autoantibodies in mice with typical AF risk factors such as hypertension, obesity, and mitral regurgitation [3]. - The use of anti-CD20 monoclonal antibodies to target and deplete B cells significantly reduced the incidence of AF in the HOMER mouse model, suggesting a new therapeutic avenue for patients with autoantibody-induced AF [6][9]. Group 2: Mechanisms of Action - In the HOMER mouse model, dendritic cells and B cells were found to expand in the left atrium and cardiac draining lymph nodes, with myocardial cell-derived proteins detected in these areas. Systemic expansion of B cells under interferon-α stimulation led to the production of autoantibodies that impaired calcium handling in myocardial cells [6]. - The depletion of B cells or inhibition of plasma cell maturation resulted in a significant reduction in the likelihood of AF being induced, highlighting the role of these immune cells in the pathophysiology of AF [7].