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<p>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&#xa0;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.</p>

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B lymphocytes contribute Angiotensin II induced cardiac hypertrophy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月8日

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  • Xiujuan Zhao,
  • Xiaoyan Di,
  • Hangli Wu,
  • Chune Fang,
  • Chunfeng Zhu,
  • Ting Yue,
  • Dan Zhang,
  • Huixiao Jia,
  • Jingsha Zhao,
  • Dong Liang,
  • Jing Liu,
  • Xinru Gao,
  • Yuanyuan Hao

摘要

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.