ArticleBiophysical journal2003
A mathematical model of the electrophysiological alterations in rat ventricular myocytes in type-I diabetes.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Cardiac digital twins: a tool to investigate the function and treatment of the diabetic heart.Cardiovascular diabetology · 2025Review
- Review
- CaBiophysical journal · 2020Article
- Hyperglycemia-induced cardiac contractile dysfunction in the diabetic heart.Heart failure reviews · 2018Review
- Altered Left Ventricular Ion Channel Transcriptome in a High-Fat-Fed Rat Model of Obesity: Insight into Obesity-Induced Arrhythmogenesis.Journal of obesity · 2016Article
- Computational analysis of the regulation of Ca(2+) dynamics in rat ventricular myocytes.Physical biology · 2015Article
- Reduced Na⁺ current density underlies impaired propagation in the diabetic rabbit ventricle.Journal of molecular and cellular cardiology · 2014Article
- Depolarization-induced automaticity in rat ventricular cardiomyocytes is based on the gating properties of L-type calcium and slow Kv channels.European biophysics journal : EBJ · 2013Article
- The force-frequency relationship: insights from mathematical modeling.Advances in physiology education · 2013Review
- How the Hodgkin-Huxley equations inspired the Cardiac Physiome Project.The Journal of physiology · 2012Article
- The chronic effects of neonatal alloxan-induced diabetes mellitus on ventricular myocyte shortening and cytosolic Ca2+.Molecular and cellular biochemistry · 2011Article
- Altered gene expression may underlie prolonged duration of the QT interval and ventricular action potential in streptozotocin-induced diabetic rat heart.Molecular and cellular biochemistry · 2009Article
- Ca/calmodulin kinase II differentially modulates potassium currents.Circulation. Arrhythmia and electrophysiology · 2009Article
- Effects of streptozotocin-induced diabetes on connexin43 mRNA and protein expression in ventricular muscle.Molecular and cellular biochemistry · 2008Article
- Effects of streptozotocin-induced diabetes on action potentials in the sinoatrial node compared with other regions of the rat heart.Molecular and cellular biochemistry · 2007Article
- Safety and efficacy of catheter ablation of atrial fibrillation in patients with diabetes mellitus--single center experience.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2006Article
- Effects of carbenoxolone on heart rhythm, contractility and intracellular calcium in streptozotocin-induced diabetic rat.Molecular and cellular biochemistry · 2006Article
- Computational biology in the study of cardiac ion channels and cell electrophysiology.Quarterly reviews of biophysics · 2006Review
- Interpretation of relevance of sodium-calcium exchange in action potential of diabetic rat heart by mathematical model.Molecular and cellular biochemistry · 2005Article
- A mathematical treatment of integrated Ca dynamics within the ventricular myocyte.Biophysical journal · 2004Article
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3 authors.
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Abstract
Our mathematical model of the rat ventricular myocyte (Pandit et al., 2001) was utilized to explore the ionic mechanism(s) that underlie the altered electrophysiological characteristics associated with the short-term model of streptozotocin-induced, type-I diabetes. The simulations show that the observed reductions in the Ca(2+)-independent transient outward K(+) current (I(t)) and the steady-state outward K(+) current (I(ss)), along with slowed inactivation of the L-type Ca(2+) current (I(CaL)), can result in the prolongation of the action potential duration, a well-known experimental finding. In addition, the model demonstrates that the slowed reactivation kinetics of I(t) in diabetic myocytes can account for the more pronounced rate-dependent action potential duration prolongation in diabetes, and that a decrease in the electrogenic Na(+)-K(+) pump current (I(NaK)) results in a small depolarization in the resting membrane potential (V(rest)). This depolarization reduces the availability of the Na(+) channels (I(Na)), thereby resulting in a slower upstroke (dV/dt(max)) of the diabetic action potential. Additional simulations suggest that a reduction in the magnitude of I(CaL), in combination with impaired sarcoplasmic reticulum uptake can lead to a decreased sarcoplasmic reticulum Ca(2+) load. These factors contribute to characteristic abnormal [Ca(2+)](i) homeostasis (reduced peak systolic value and rate of decay) in myocytes from diabetic animals. In combination, these simulation results provide novel information and integrative insights concerning plausible ionic mechanisms for the observed changes in cardiac repolarization and excitation-contraction coupling in rat ventricular myocytes in the setting of streptozotocin-induced, type-I diabetes.
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