ArticleMolecular and cellular biochemistry2004
Diabetes decreases mRNA levels of calcium-release channels in human atrial appendage.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Concomitant Diabetes and Atrial Fibrillation: Epicardial Fat and Macrophage-Related Mechanisms.Diabetes/metabolism research and reviews · 2025Review
- CaPflugers Archiv : European journal of physiology · 2022Review
- Investigation of the Effects and Mechanisms of Mai Tong Formula on Lower Limb Macroangiopathy in a Spontaneous Diabetic Rat Model.Journal of diabetes research · 2016Article
- 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
- Cardiac ryanodine receptor in metabolic syndrome: is JTV519 (K201) future therapy?Diabetes, metabolic syndrome and obesity : targets and therapy · 2012Article
- Endoplasmic-reticulum calcium depletion and disease.Cold Spring Harbor perspectives in biology · 2011Review
- Genetics of variation in serum uric acid and cardiovascular risk factors in Mexican Americans.The Journal of clinical endocrinology and metabolism · 2009Article
- Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes.Journal of molecular and cellular cardiology · 2008Review
- Sarcoplasmic Ca2+ release is prolonged in nonfailing myocardium of diabetic patients.Molecular and cellular biochemistry · 2008Article
- Mechanisms of impaired calcium handling underlying subclinical diastolic dysfunction in diabetes.American journal of physiology. Regulatory, integrative and comparative physiology · 2007Article
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Authors and funding
7 authors.
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Abstract
Patients with chronic diabetes mellitus usually develop reductions in rate and force of cardiac contractions. Since calcium-release channels (ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs)) play integral roles in effecting these processes, we rationalize that alterations in their expression may underlie these defects. To test this hypothesis, right atrial appendages were obtained from diabetic (65.0 ± 4.5 years) and nondiabetic (56.2 ± 2.6 years) patients undergoing coronary arterial by-pass grafting and reverse transcription-polymerase chain reactions were used to compare steady state levels of mRNA encoding the three major isoforms of RyRs and IP3Rs. In this study we did not detect either RyR1 or RyR3 in human atrial appendage. When compared with nondiabetic patients, mRNA encoding RyR2 from diabetic patients decreased by 74.2 ± 6.2% (p< 0.01). Diabetes also significantly decreased steady-state levels of mRNA encoding the IP3Rs in human atrial appendage. IP3R1 decreased by 24.2 ± 4.6%, IP3R2 decreased by 63.0 ± 4.6% and IP3R3 decreased by 55.5 ± 6.5%. Since a reduction in steady-state mRNA is usually indicative of a decrease in protein levels, these data suggest that the decrease in chronotropy and inotropy seen in chronic diabetic patients may be due in part to a decrease in expression of calcium-release channels. (Mol Cell Biochem 263: 143-150, 2004).
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