Abstract
Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both. DM is a leading cause of mortality and morbidity worldwide, with diabetic cardiomyopathy as one of its main complications. It is well established that cardiovascular complications are common in both types of diabetes. Electrical and mechanical problems, resulting in cardiac contractile dysfunction, are considered as the major complications present in diabetic hearts. Inevitably, disturbances in the mechanism(s) of Ca2+ signaling in diabetes have implications for cardiac myocyte contraction. Over the last decade, significant progress has been made in outlining the mechanisms responsible for the diminished cardiac contractile function in diabetes using different animal models of type I diabetes mellitus (TIDM) and type II diabetes mellitus (TIIDM). The aim of this review is to evaluate our current understanding of the disturbances of Ca2+ transport and the role of main cardiac proteins involved in Ca2+ homeostasis in the diabetic rat ventricular cardiomyocytes. Exploring the molecular mechanism(s) of altered Ca2+ signaling in diabetes will provide an insight for the identification of novel therapeutic approaches to improve the heart function in diabetic patients.
Highlights
Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by abnormally high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both
Significant progress has been made in outlining the mechanisms responsible for the diminished cardiac contractile function in diabetes using different animal models of type I diabetes mellitus (TIDM) and type II diabetes mellitus (TIIDM)
The aim of this review is to evaluate our current understanding of the disturbances of Ca2+ transport and the role of main cardiac proteins involved in Ca2+ homeostasis in the diabetic rat ventricular cardiomyocytes
Summary
Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by abnormally high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both. Upregulation of the gene encoding the α1 subunit of the Cav1.2 ion channel (Cacna1c) may provide an early compensatory mechanism for the reduced density and prolonged inactivation of the L-type Ca2+ current demonstrated in myocytes from Zucker diabetic fatty rat compared to their respective controls [31]. In contrast to these findings, recent studies on the Goto–Kakizaki (GK) rat, a nonobese genetic model of TIIDM, have shown no change in the Ltype Ca2+ channel activity in ventricular myocytes [32, 33].
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