B lymphocytes contribute Angiotensin II induced cardiac hypertrophy.

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 inflam

SUBMITTER: Zhao X 

PROVIDER: S-EPMC12685947 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature