ArticleDiabetes2008
Altered calcium homeostasis does not explain the contractile deficit of diabetic cardiomyopathy.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- Cardiac remodelling in type 2 diabetes: Pathophysiological mechanisms and opportunities for multiscale computational modelling and simulation.The Journal of physiology · 2026Review
- Myocardial composition and contractile function of right atrial trabeculae from type 2 diabetic and nondiabetic male patients.Physiological reports · 2025Article
- Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin.Frontiers in physiology · 2025Article
- Sacubitril/Valsartan Combination Partially Improves Cardiac Systolic, but Not Diastolic, Function through β-AR Responsiveness in a Rat Model of Type 2 Diabetes.International journal of molecular sciences · 2024Article
- Impaired calcium handling mechanisms in atrial trabeculae of diabetic patients.Physiological reports · 2023Article
- Sarco/endoplasmic reticulum calcium ATPase activity is unchanged despite increased myofilament calcium sensitivity in Zucker type 2 diabetic fatty rat heart.Scientific reports · 2022Article
- Systolic Dysfunction of the Heart in Type 1 Diabetes Mellitus.Bulletin of experimental biology and medicine · 2021Article
- STZ-diabetic rat heart maintains developed tension amplitude by increasing sarcomere length and crossbridge density.Experimental physiology · 2021Article
- Quantitative high-throughput assay to measure MC4R-induced intracellular calcium.Journal of molecular endocrinology · 2021Article
- Pim-1 Kinase Phosphorylates Cardiac Troponin I and Regulates Cardiac Myofilament Function.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
- The Rho kinase inhibitor, fasudil, ameliorates diabetes-induced cardiac dysfunction by improving calcium clearance and actin remodeling.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Removal of Abnormal Myofilament O-GlcNAcylation Restores Ca2+ Sensitivity in Diabetic Cardiac Muscle.Diabetes · 2015Article
- Examination of the Effects of Heterogeneous Organization of RyR Clusters, Myofibrils and Mitochondria on Ca2+ Release Patterns in Cardiomyocytes.PLoS computational biology · 2015Article
- Restoring redox balance enhances contractility in heart trabeculae from type 2 diabetic rats exposed to high glucose.American journal of physiology. Heart and circulatory physiology · 2015Article
- Mechanisms underlying the impaired contractility of diabetic cardiomyopathy.World journal of cardiology · 2014Review
- Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelation.Cardiovascular diabetology · 2014Article
- Streptozotocin-induced diabetes prolongs twitch duration without affecting the energetics of isolated ventricular trabeculae.Cardiovascular diabetology · 2014Article
- A novel role for SIRT-1 in L-arginine protection against STZ induced myocardial fibrosis in rats.PloS one · 2014Article
- Significance of AT1 receptor independent activation of mineralocorticoid receptor in murine diabetic cardiomyopathy.PloS one · 2014Article
- Protection of the heart by treatment with a divalent-copper-selective chelator reveals a novel mechanism underlying cardiomyopathy in diabetic rats.Cardiovascular diabetology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study examines the extent to which the contractile deficit of diabetic cardiomyopathy is due to altered Ca(2+) homeostasis. RESEARCH DESIGN AND
methodsMeasurements of isometric force and intracellular calcium ([Ca(2+)](i), using fura-2/AM) were made in left ventricular (LV) trabeculae from rats with streptozotocin-induced diabetes and age-matched siblings.
resultsAt 1.5 mmol/l [Ca(2+)](o), 37 degrees C, and 5-Hz stimulation frequency, peak stress was depressed in diabetic rats (10 +/- 1 vs. 17 +/- 2 mN/mm(2) in controls; P < 0.05) with a slower time to peak stress (77 +/- 3 vs. 67 +/- 2 ms; P < 0.01) and time to 90% relaxation (76 +/- 7 vs. 56 +/- 3 ms; P < 0.05). No difference was found between groups for either resting or peak Ca(2+), but the Ca(2+) transient was slower in time to peak (39 +/- 2 vs. 34 +/- 1 ms) and decay (time constant, 61 +/- 3 vs. 49 +/- 3 ms). Diabetic rats had a longer LV action potential (APD(50), 98 +/- 5 vs. 62 +/- 5 ms; P < 0.0001). Western blotting showed that diabetic rats had a reduced expression of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA)2a, with no difference in expression of the Na(+)/Ca(2+) exchanger. Immunohistochemistry of LV free wall showed that type I collagen was increased in diabetic rats (diabetic 7.1 +/- 0.1%, control 12.7 +/- 0.1%; P < 0.01), and F-actin content reduced (diabetic 56.9 +/- 0.6%; control 61.7 +/- 0.4%; P < 0.0001) with a disrupted structure.
conclusionsWe find no evidence to support the idea that altered Ca(2+) homeostasis underlies the contractile deficit of diabetic cardiomyopathy. The slower action potential and reduced SERCA2a expression can explain the slower Ca(2+) transient kinetics in diabetic rats but not the contractile deficit. Instead, we suggest that the observed LV remodeling may play a crucial role.
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