Key result
Pre-MI exercise training improves post-MI LV function and suppresses B-cell infiltration in mice.
Why the study?
Although B lymphocytes play a crucial role in MI progression, the existence, unique phenotype, and function of B lymphocytes in response to physical exercise after MI remain poorly understood.
Does 2 months of prior exercise training improve left ventricular function and reduce myocardial injury and B-cell infiltration in mice after myocardial infarction?
Does 2 months of prior exercise training improve left ventricular function and reduce myocardial injury and B-cell infiltration in mice after myocardial infarction?
In a mouse model of myocardial infarction, pre-infarction exercise training protects cardiac function and reduces fibrosis by downregulating the CXCL13-CXCR5 axis to limit B-cell infiltration and decreasing B-cell granzyme B release.
Exercise-induced B-cell mobilization post-MI observed in animals; leaves open human relevance and therapeutic translation.
Background Emerging evidence suggests that B lymphocytes play a crucial role in the progression of myocardial infraction. However, the existence, unique phenotype and function of B lymphocytes in response to physical exercise after MI remain poorly understood. Objective This study aimed to investigate the mechanism underlying exercise training-induced mobilization of B lymphocytes to the myocardium after myocardial infraction and to examine the activation, cytokine secretion, and autoantibody production of B lymphocytes in response to exercise training. Additionally, we sought to determine whether this mechanism contributes to the protective effects against MI. Methods and Results An 8-week-old C57BL/6J mouse model was used, with mice randomly assigned to sedentary control or exercise training groups. After 2 months of training, MI was induced by permanent left coronary artery ligation, and parameters were assessed at 3 and 21 days post-MI. Sedentary mice showed reduced left ventricular function, increased cardiomyocyte apoptosis, and leukocyte infiltration, whereas exercise-trained mice exhibited significant improvement in these measures. Further experiments revealed that exercise-driven B lymphocytes mediated the cardioprotective effects of exercise. Exercise reduced myocardial CXCL13 expression and CXCR5 levels on B cells, leading to decreased B-cell infiltration. Transfer of CXCR5-deficient or exercise-derived B cells into μMT⁻/⁻ mice reduced cardiac fibrosis and inflammation and improved cardiac function after MI. Moreover, B cells lacking granzyme B alleviated post-MI remodeling, and transfer of anti-CD19-CAR-NK cells protected cardiac function by inhibiting B cells. Conclusions Physical exercise exerted a protective effect against MI by regulating B lymphocytes infiltration in the heart. This protection is mediated through the downregulation of CXCL13 expression in the myocardium and reduced CXCR5 levels on B lymphocytes, thereby limiting B-cell recruitment after MI. In addition, exercise training decreases granzyme B release from B cells, attenuating myocardial injury and improves heart function. These findings highlight therapeutic potential of targeting B lymphocytes and their receptors to enhance the cardioprotective benefits of exercise following MI.
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Liu et al. (2026) studied Myocardial infarction (preclinical mouse model). Exercise training vs. Sedentary control was evaluated on Left ventricular function, cardiomyocyte apoptosis, leukocyte and B-cell infiltration, and post-MI cardiac remodeling. Exercise training for 2 months prior to MI improved LV function and reduced B-cell infiltration via CXCL13/CXCR5 downregulation at 3 and 21 days post-MI in mice.
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