Gene Therapy’s Future for Treatment of Myocardial Infarction (original) (raw)

M ore than 1 million Americans experience new or recurrent myocardial infarction (MI) annually 1 with clinical outcomes strongly related to infarct size and the deleterious effects of ventricular remodeling. 2,3 Standard MI treatments are appropriately directed at early reperfusion, antiplatelet/ lipid-lowering therapies, and the administration of β-blockers and angiotensin-converting enzyme inhibitors to help reduce adverse post-MI ventricular remodeling. However, there is strong evidence to suggest that inflammation and the generation of reactive oxygen species, such as the superoxide anion (O 2 − ), contribute substantially to myocardial ischemia/ reperfusion injury. 4 Thus, there is great interest in developing novel therapies targeting postinfarct inflammatory processes, including oxidative stress.

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