Abstract
Immune responses play a critical role in myocardial injury, yet the specific contribution of B lymphocyte-dependent mechanisms to Angiotensin Ⅱ (Ang Ⅱ)-induced cardiac hypertrophy remains largely undefined. We hypothesized that B cells promote pathological remodeling by regulating chemokine production and monocyte recruitment. To investigate this hypothesis, wild-type (WT) and B cell-deficient (µMT) mice were infused with Ang II (1.5 µg/g/day) for 2 or 4 weeks. Blood pressure measurement, echocardiography, flow cytometry, and histopathology were performed to assess cardiac remodeling and inflammation. We found that following Ang II treatment, B lymphocytes selectively produced CCL7, which facilitated the mobilization and recruitment of Ly6C⁺ monocytes into the myocardium, leading to inflammation, tissue injury, and hypertrophy. In contrast, genetic ablation of B cells markedly reduced CCL7 production, limited monocyte infiltration, and attenuated cardiac hypertrophy, despite similar blood pressure responses. Consistently, mice with a B cell-specific deficiency of CCL7 exhibited comparable protective effects. Our findings demonstrate that B lymphocytes critically amplify Ang Ⅱ-induced cardiac hypertrophy by producing CCL7 and promoting monocyte recruitment. This B cell-dependent mechanism operates independently of hypertension and identifies B cell-mediated inflammation as a potential therapeutic target in hypertensive heart disease.