Abstract
Type 1 diabetes is commonly associated with an elevated level of reactive carbonyl species in serum due to alteration of glucose and fatty acid metabolism. Diabetic cardiomyocytes are also characterized by abnormal intracellular Ca2+ regulation. Here, we studied how carbonylation of ion channels and pumps by methylglyoxal (MGO) affects Ca2+ regulation in mouse ventricular myocytes. Analysis of cytosolic Ca2+ dynamics revealed that MGO (200 μM) increases the action potential-induced Ca2+ transients and sarcoplasmic reticulum (SR) Ca2+ load, with a limited effect on L-type Ca2+ channels and SERCA-mediated Ca2+ uptake.
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