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Coronary artery disease (CAD), including its acute manifestations such as myocardial infarction (MI), is one of the leading causes of morbidity and mortality worldwide,1 especially in countries where the development of atherosclerotic plaques is closely linked to certain dietary habits (ie, Western diet).2 For decades, research has focused on deciphering the detailed mode(s) of disease development and implementing appropriate prevention and treatment strategies. A widely used model systems for the induction and development of atherosclerotic lesions, which augments studies in the Apoe−/− mouse, is the Ldlr−/− mouse strain.3 This genetically manipulated murine model is characterized by elevated plasma cholesterol levels with the development of atherosclerotic plaques under specific dietary conditions. However, these animals do not develop spontaneous atherosclerotic lesions or plaques.Article, see p 213 In addition to these murine model systems, in recent years, human genome-wide association studies for CAD/MI have identified associations between increased CAD disease prevalence and distinct gene loci. Among others, a 58-kb risk locus on chromosome 9p21.3 was identified and further characterized as being associated with the severity of CAD, but not of MI.4–6 The locus was linked to primary effects on atherogenesis, rather than on acute plaque rupture causing MI.7 Furthermore, investigations of an expanded 500-kb region, which confirmed the 58-kb CAD core block, …

Cdkn2a Orchestrates Platelet Production and Reactivity in Atherosclerosis