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<p>Microvascular obstruction (MVO) is a fundamental mechanism underlying the occurrence of no-reflow, which contributes to myocardial ischemia–reperfusion injury (MI/RI). Despite its significance, the precise pathophysiology of MVO remains incompletely understood. In this study, we aim to investigate the role of CD80/86, co-stimulatory molecules crucial for T cell activation, in exacerbating MVO during MI/RI, and elucidate their potential mechanism of action. The results revealed a significant increase in cardiac CD80/86 in mice after I/R treatment. Strikingly, the deletion of CD80/86 greatly improved cardiac function, reduced infarct size, and mitigated apoptosis 24&#xa0;h after MI/R. Mechanistically, CD80/86 deletion or inhibition led to a reduction in E-selectin expression, subsequently decreasing the infiltration of macrophages and T cells, thereby counteracting MVO and ameliorating the development of no-reflow during MI/RI. In conclusion, our data highlight the crucial involvement of CD80/86 in regulating macrophage and T cells infiltration, leading to the alleviation of MVO and myocardial MI/RI. The insights gained from this study suggest that targeted inhibition of CD80/86 holds promise as a potential therapeutic strategy to protect cardiac function in patients with acute myocardial infarction undergoing reperfusion therapy. Further research in this direction could pave the way for improved treatment options in the management of ischemic heart conditions.</p>

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Attenuation of myocardial ischemia–reperfusion injury in mice through CD80/86 deficiency: improved microvascular obstruction via reduced macrophage and T lymphocyte infiltration

  • 期刊论文

  • 发表日期：

    2025年8月1日

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  • Lu Liu,
  • Xiao-Xiao Wang,
  • Si-Xue Wang,
  • Hui Yang,
  • Xue Xiao,
  • Nan Li,
  • Hao-Jiang Chai,
  • Hong-Xia Wang

摘要

Microvascular obstruction (MVO) is a fundamental mechanism underlying the occurrence of no-reflow, which contributes to myocardial ischemia–reperfusion injury (MI/RI). Despite its significance, the precise pathophysiology of MVO remains incompletely understood. In this study, we aim to investigate the role of CD80/86, co-stimulatory molecules crucial for T cell activation, in exacerbating MVO during MI/RI, and elucidate their potential mechanism of action. The results revealed a significant increase in cardiac CD80/86 in mice after I/R treatment. Strikingly, the deletion of CD80/86 greatly improved cardiac function, reduced infarct size, and mitigated apoptosis 24 h after MI/R. Mechanistically, CD80/86 deletion or inhibition led to a reduction in E-selectin expression, subsequently decreasing the infiltration of macrophages and T cells, thereby counteracting MVO and ameliorating the development of no-reflow during MI/RI. In conclusion, our data highlight the crucial involvement of CD80/86 in regulating macrophage and T cells infiltration, leading to the alleviation of MVO and myocardial MI/RI. The insights gained from this study suggest that targeted inhibition of CD80/86 holds promise as a potential therapeutic strategy to protect cardiac function in patients with acute myocardial infarction undergoing reperfusion therapy. Further research in this direction could pave the way for improved treatment options in the management of ischemic heart conditions.