Key result
Defective calcium homeostasis drives diabetic cardiac dysfunction and arrhythmogenesis via altered RyR2, SERCa2a, and NCX1.
This review highlights the role of calcium homeostasis remodeling in diabetic cardiomyopathy and arrhythmogenesis, suggesting Ca2+ handling proteins as potential therapeutic targets.
Positions Ca2+ handling proteins as potential targets in diabetic cardiomyopathy; leaves open confirmation in prospective trials.
A rapid growth in the incidence of diabetes and obesity has transpired to a major heath issue and economic burden in the postindustrial world, with more than 29 million patients affected in the United States alone. Cardiovascular defects have been established as the leading cause of mortality and morbidity of diabetic patients. Over the last decade, significant progress has been made in delineating mechanisms responsible for the diminished cardiac contractile function and enhanced propensity for malignant cardiac arrhythmias characteristic of diabetic disease. Rhythmic cardiac contractility relies upon the precise interplay between several cellular Ca 2+ transport protein complexes including plasmalemmal L-type Ca 2+ channels (LTCC), Na + -Ca 2+ exchanger (NCX1), Sarco/endoplasmic Reticulum (SR) Ca 2+ -ATPase (SERCa2a) and ryanodine receptors (RyR2s), the SR Ca 2+ release channels. Here we provide an overview of changes in Ca 2+ homeostasis in diabetic ventricular myocytes and discuss the therapeutic potential of targeting Ca 2+ handling proteins in the prevention of diabetes-associated cardiomyopathy and arrhythmogenesis.
No takes yet. Share an insight, caveat, or question.
Hamilton et al. (2018) conducted a review in Diabetes and Obesity-related Cardiac Disease. Defective intracellular calcium homeostasis, driven by alterations in key handling proteins like RyR2, SERCa2a, and NCX1, is a major contributor to diabetes-related cardiac dysfunction and arrhythmogenesis.