ArticleCardiovascular research2011
Gain of function of cardiac ryanodine receptor in a rat model of type 1 diabetes.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and dysfunction of RyR2 in the heart of streptozotocin-induced diabetic rats.BMC cardiovascular disorders · 2024Article
- Type 1 diabetes, its complications, and non-ischemic cardiomyopathy: a mendelian randomization study of European ancestry.Cardiovascular diabetology · 2024Article
- Diabetes-induced chronic heart failure is due to defects in calcium transporting and regulatory contractile proteins: cellular and molecular evidence.Heart failure reviews · 2023Review
- HIV-Tat Exacerbates the Actions of Atazanavir, Efavirenz, and Ritonavir on Cardiac Ryanodine Receptor (RyR2).International journal of molecular sciences · 2022Article
- Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and ameliorates inflammation in the lung of streptozotocin-induced diabetic rats.Pharmaceutical biology · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- Calcium signaling in endocardial and epicardial ventricular myocytes from streptozotocin-induced diabetic rats.Journal of diabetes investigation · 2021Article
- Efavirenz, atazanavir, and ritonavir disrupt sarcoplasmic reticulum CaAntiviral research · 2021Article
- Calcium Homeostasis in Ventricular Myocytes of Diabetic Cardiomyopathy.Journal of diabetes research · 2020Review
- Gender-Dependent Alteration of CaFrontiers in physiology · 2019Article
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- Cardiac-specific suppression of NF-κB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system.American journal of physiology. Heart and circulatory physiology · 2014Article
- CCDI: a new ligand that modulates mammalian type 1 ryanodine receptor (RyR1).British journal of pharmacology · 2014Article
- Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca(2+) signaling pathway.World journal of biological chemistry · 2014Review
- Reactive carbonyl species and their roles in sarcoplasmic reticulum Ca2+ cycling defect in the diabetic heart.Heart failure reviews · 2014Review
- Trace elements in diabetic cardiomyopathy: An electrophysiological overview.World journal of diabetes · 2013Article
- Dust from hog confinement facilities impairs Ca2+ mobilization from sarco(endo)plasmic reticulum by inhibiting ryanodine receptors.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Zinc-induced cardiomyocyte relaxation in a rat model of hyperglycemia is independent of myosin isoform.Cardiovascular diabetology · 2012Article
- Role of oxidative stress and Ca²⁺ signaling on molecular pathways of neuropathic pain in diabetes: focus on TRP channels.Neurochemical research · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
aimsVentricular myocytes isolated from hearts of streptozotocin (STZ)-diabetic rats exhibit increased spontaneous Ca(2+) release. Studies attribute this defect to an enhancement in activity of type 2 ryanodine receptor (RyR2). To date, underlying reasons for RyR2 dysregulation remain undefined. This study assesses whether the responsiveness of RyR2 following stimulation by intrinsic ligands is being altered during experimental type 1 diabetes (T1D). METHODS AND
resultsM-mode echocardiography established a cardiomyopathy in 8 weeks STZ-diabetic rats. Confocal microscopy confirmed an increase in the spontaneous Ca(2+) release in isolated ventricular myocytes. Western blots revealed no significant change in steady-state levels of the RyR2 protein. When purified to homogeneity and incorporated into planar lipid bilayers, RyR2 from STZ-diabetic rats (dRyR2) exhibited reduced current amplitude at ±35 mV. dRyR2 was also more responsive to intrinsic cytoplasmic activators Ca(2+), adenosine triphosphate, and cyclic adenosine diphosphate ribose and less responsive to the cytoplasmic deactivator Mg(2+). Threshold for the activation of RyR2 by trans (luminal) Ca(2+) was also reduced. These changes were independent of phosphorylation at Ser2808 and Ser2814. Two weeks of insulin treatment starting after 6 weeks of diabetes blunted the phenotype change, indicating that the gain of function is specific to the diabetes and not the result of STZ interacting directly with RyR2.
conclusionThese data show, for the first time, that RyR2 is acquiring a gain-of-function phenotype independent of its phosphorylation status during T1D and provides new insights for the enhanced spontaneous Ca(2+) release in myocytes from T1D rats.
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