Why the study?
Mortality from cardiac rupture after acute MI remains high despite advances in reperfusion strategies, and the relevance of thrombolytic therapy as an accelerating risk factor remains controversial.
Does Par4 deletion affect cardiac remodeling, inflammation resolution, and cardiac rupture incidence after myocardial infarction in mice?
Does Par4 deletion affect cardiac remodeling, inflammation resolution, and cardiac rupture incidence after myocardial infarction in mice?
Par4 plays an essential role in inflammation resolution during myocardial healing, indicating that long-term Par4 inhibition after MI should be avoided.
BACKGROUND: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk factor remains controversial. METHODS: We analyzed protease-activated receptor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistry, and flow cytometry. RESULTS: mice restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function after MI. CONCLUSIONS: These findings reveal essential roles of Par4 in neutrophil apoptosis and inflammation resolution during myocardial healing and point to Par4 inhibition as a potential therapy that should be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.
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Kolpakov et al. (2020) studied this question.
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