Nukala SB, Regazzoni L, Aldini G, et al. - Researchers assessed the cellular mechanisms of endothelial dysfunction in patients with acute myocardial infarction (AMI), for the first time ever, in this quantitative proteomics study. Of 2,246 proteins that were identified and quantified, 335 were differentially regulated in coronary arterial endothelial cells from patients with AMI vs controls. They found that change of metabolism of RNA, platelet activation, signaling, and aggregation, neutrophil degranulation, metabolism of amino acids and derivatives, cellular responses to stress, and response to elevated platelet cytosolic Ca²⁺ pathways, was revealed by differentially regulated protein profiles. The involvement of oxidative stress as a mediator of endothelial dysfunction during AMI was suggested by the observed enhanced generation of oxidants and reduced production of antioxidant biomarkers as well as downregulation of proteins with antioxidant properties.