Diabetic cardiomyopathy (DCM) is a serious diabetes-associated complication that results in myocardial dysfunction independent of other etiological factors [1]. Pathological alterations to the myocardium associated with DCM include circulatory defects, impaired heart muscle contraction, and abnormal calcium (Ca2+) homeostasis in cardiac cells[2]. In myocardium, endothelial cells play an essential role in maintaining intracellular Ca2+ hemostasis in response to stimuli and regulating cardiac function [3]. External stimulus may cause abrupt changes in Ca2+ balance, including Ca2+ release from sarco-endoplasmic reticulum (ER) [4]. Subsequent return of the Ca2+ level to basal levels occurs due to Ca2+ decay mechanism, which is mainly regulated by sarco-endoplasmic reticulum Ca2+ ATPase pumps (SERCA) present at ER membrane which are responsible for Ca2+ sequestration [5]. Studies have shown that the mechanisms by which Ca2+ homeostasis alters cardiac function in diabetic cardiomyocytes include reduced activity of the SERCA pumps [6]. However, no information is available regarding the effects of diabetes on Ca2+ hemostasis and the underlying Ca2+ sequestration mechanism in diabetic cardiac endothelial cells[7]. This study tested the hypothesis that diabetic endothelial cells will exhibit disruptions in Ca2+ decay kinetics via alterations in the sequestration mechanism.

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