Exogenous CXCL4 worsens post-myocardial infarction outcomes by impairing macrophage phagocytosis and increasing mortality and LV dilation.
Animal data position CXCL4 as post-MI target; leaves open clinical translation and human trials.
CXCL4 infusion impaired macrophage phagocytic capacity by reducing CD36 levels through MMP-9 dependent and independent signalling, leading to higher mortality and LV dilation.
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Lindsey et al. (2018) studied this question.
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