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Role of endothelin‐1, sodium hydrogen exchanger‐1 and mitogen activated protein kinase (MAPK) activation in glucose‐induced cardiomyocyte hypertrophy

Cardiac hypertrophy is a key structural feature of diabetic cardiomyopathy. Previous studies have shown that diabetes‐induced endothelin‐1 (ET‐1) and sodium hydrogen exchanger‐1 (NHE‐1) mediate structural and functional deficits in the heart. In order to gain a mechanistic understanding of the role of ET‐1 and NHE‐1 in cardiomyocyte hypertrophy, we have utilized an in vitro endothelial‐myocyte co‐culture system to reveal cellular interactions that may arbitrate cardiomyocyte deficits in diabetes.