Diabetic cardiomyopathy (DCM) is a serious diabetes-associated complication that results in myocardial dysfunction independent of other etiological factors . Pathological alterations to the myocardium associated with DCM include circulatory defects, impaired heart muscle contraction, and abnormal calcium (Ca2+) homeostasis in cardiac cells. In myocardium, endothelial cells play an essential role in maintaining intracellular Ca2+ hemostasis in response to stimuli and regulating cardiac function . External stimulus may cause abrupt changes in Ca2+ balance, including Ca2+ release from sarco-endoplasmic reticulum (ER) . 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 . Studies have shown that the mechanisms by which Ca2+ homeostasis alters cardiac function in diabetic cardiomyocytes include reduced activity of the SERCA pumps . However, no information is available regarding the effects of diabetes on Ca2+ hemostasis and the underlying Ca2+ sequestration mechanism in diabetic cardiac endothelial cells. This study tested the hypothesis that diabetic endothelial cells will exhibit disruptions in Ca2+ decay kinetics via alterations in the sequestration mechanism.
- Bioengineering Division
Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells
- Views Icon Views
- Share Icon Share
- Search Site
Sheikh, AQ, Hurley, JR, & Narmoneva, DA. "Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells." Proceedings of the ASME 2011 Summer Bioengineering Conference. ASME 2011 Summer Bioengineering Conference, Parts A and B. Farmington, Pennsylvania, USA. June 22–25, 2011. pp. 201-202. ASME. https://doi.org/10.1115/SBC2011-53797
Download citation file: