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Increased Nox2 in cardiomyocytes after acute myocardial infarction

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For the first time, researchers have identified Nox2 within human cardiomyocytes and shown that its expression increases during acute myocardial infarction.

Nox2 is an enzymatic subunit of phagocytic NADPH oxidase. It is a cell specific source of reactive oxygen species (ROS), which in turn can induce cell damage, proliferation, apoptosis, gene expression, and aging.

Investigators from the University of Amsterdam examined cardiomyocytes from infarcted and non-infarcted areas of the hearts of patients dying after an acute myocardial infarct as well as from controls without known heart disease. Western blotting and immunohistochemical techniques proved that Nox2 was present in the plasma membrane and cytosol of cardiomyocytes. It was expressed more in infarcted than in control areas. This upregulation is probably related to production of ROS so may well play an important role in cell damage. Its precise pathophysiological role is ripe for further study.

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