Red blood cells (RBCs) play an important role in the cardiac ischemia/reperfusion (I/R) injury. Cardiovascular risk factors impair the RBC function in an endothelial nitric oxide synthase (eNOS) dependent manner. However, it is unclear whether the protective role of RBCs can be rescued by modifying cardiovascular risk factors or by pharmacologic intervention.
View Article and Find Full Text PDFIntroduction: Myocardial infarction is one of the leading causes of morbidity and mortality worldwide. Cellular interactions of red blood cells (RBCs) and platelets with endothelial cells and cardiomyocytes play a crucial role in cardiac ischemia/reperfusion (I/R) injury. However, addressing the specific impact of such cell-to-cell interactions in commonly employed in vivo models of cardiac I/R injury is challenging due to overlap of neuronal, hormonal, and immunological pathways.
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