OLR1 and acute myocardial infarction: In summary, genetic alterations favoring LOXIN isoform production coupled to the observation that this isoform exerts a dominant-negative effect on LOX-1 function make it an attractive new target for prevention and treatment of initiation, progression, and clinical consequences of atherosclerosis such as plaque instability, acute myocardial infarction, and ischemia reperfusion injury.