ArticleMolecular and cellular biochemistry2008
Sarcoplasmic Ca2+ release is prolonged in nonfailing myocardium of diabetic patients.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Effects of Obesity and Diabesity on Ventricular Muscle Structure and Function in the Zucker Rat.Life (Basel, Switzerland) · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation.Cardiovascular research · 2021Review
- Atrial remodeling and atrial fibrillation in acquired forms of cardiovascular disease.Heart rhythm O2 · 2020Article
- Calcium Homeostasis in Ventricular Myocytes of Diabetic Cardiomyopathy.Journal of diabetes research · 2020Review
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- The Type 2 Diabetic Heart: Its Role in Exercise Intolerance and the Challenge to Find Effective Exercise Interventions.Sports medicine (Auckland, N.Z.) · 2016Review
- The role of CaMKII in diabetic heart dysfunction.Heart failure reviews · 2015Review
- Intracellular Zinc Modulates Cardiac Ryanodine Receptor-mediated Calcium Release.The Journal of biological chemistry · 2015Article
- How exercise may amend metabolic disturbances in diabetic cardiomyopathy.Antioxidants & redox signaling · 2015Review
- Impaired relaxation despite upregulated calcium-handling protein atrial myocardium from type 2 diabetic patients with preserved ejection fraction.Cardiovascular diabetology · 2014Article
- Reactive carbonyl species and their roles in sarcoplasmic reticulum Ca2+ cycling defect in the diabetic heart.Heart failure reviews · 2014Review
- Endoplasmic-reticulum calcium depletion and disease.Cold Spring Harbor perspectives in biology · 2011Review
- The chronic effects of neonatal alloxan-induced diabetes mellitus on ventricular myocyte shortening and cytosolic Ca2+.Molecular and cellular biochemistry · 2011Article
- Diabetes-related defects in sarcoplasmic Ca2+ release are prevented by inactivation of G(alpha)11 and G(alpha)q in murine cardiomyocytes.Molecular and cellular biochemistry · 2010Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Asymptomatic diabetic patients have a high incidence of clinically unrecognized left ventricular dysfunction with an abnormal cardiac response to exercise. We, therefore, examined subclinical defects in the contraction-relaxation cycle and intracellular Ca(2+) regulation in myocardium of asymptomatic type 2 diabetic patients. Methods Alterations in the dynamics of the intracellular Ca(2+) transient and contractility were recorded in right atrial myocardium of type 2 diabetic patients and non-diabetic control tissue loaded with fura-2. In order to gain an insight into mechanisms underlying the altered Ca(2+) handling in diabetic myocardium levels of mRNA, protein expression and phosphorylation of key proteins in sarcoplasmic Ca(2+) handling were determined. Results In isolated atrial trabeculae of diabetic myocardium the rise of systolic Ca(2+) was significantly prolonged, but relaxation of the Ca(2+) transient was unaltered compared to control tissue. Accordingly, the levels of expression of mRNA and protein of the Ca(2+) release channel (RyR2) of the sarcoplasmic reticulum were reduced by 68 and 22%, respectively. Endogenous phosphorylation of RyR2 by protein kinases C, however, was increased by 31% in diabetic myocardium, as assessed by the back-phosphorylation technique. Levels of expression of SERCA2 and phospholamban were unaltered between both groups. Conclusions Intracellular Ca(2+) release is prolonged in non-failing myocardium of type 2 diabetic patients and this may be primarily due to a decreased expression of RyR2. This defective Ca(2+) release may represent an early stage of ventricular dysfunction in type 2 diabetes and would favor the abnormal response to exercise frequently observed in asymptomatic diabetic patients.
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