scholarly article | Q13442814 |
P50 | author | E. Dale Abel | Q59100279 |
Angelica López-Izquierdo | Q60558840 | ||
P2093 | author name string | Adam R Wende | |
Martin Tristani-Firouzi | |||
Bonnie B Punske | |||
Renata O Pereira | |||
P2860 | cites work | Diabetic cardiomyopathy: electromechanical cellular alterations | Q80473302 |
Cardiac hypertrophy caused by peroxisome proliferator- activated receptor-gamma agonist treatment occurs independently of changes in myocardial insulin signaling | Q81152659 | ||
Targeted deletion of Kv4.2 eliminates I(to,f) and results in electrical and molecular remodeling, with no evidence of ventricular hypertrophy or myocardial dysfunction | Q81492019 | ||
Diabetic cardiomyopathy | Q82636239 | ||
Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart | Q24562618 | ||
Regulation of KChIP2 potassium channel beta subunit gene expression underlies the gradient of transient outward current in canine and human ventricle | Q24647258 | ||
Transmural expression of transient outward potassium current subunits in normal and failing canine and human hearts | Q24676825 | ||
The molecular physiology of the cardiac transient outward potassium current (I(to)) in normal and diseased myocardium | Q28188047 | ||
Augmentation of Kv4.2-encoded currents by accessory dipeptidyl peptidase 6 and 10 subunits reflects selective cell surface Kv4.2 protein stabilization | Q28590262 | ||
Spatial distributions of Kv4 channels and KChip2 isoforms in the murine heart based on laser capture microdissection | Q33272893 | ||
Molecular determinants of cardiac transient outward potassium current (I(to)) expression and regulation | Q33618573 | ||
Diabetic cardiomyopathy, causes and effects | Q34038623 | ||
Co-assembly of Kv4 {alpha} subunits with K+ channel-interacting protein 2 stabilizes protein expression and promotes surface retention of channel complexes | Q34236486 | ||
Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload | Q34502029 | ||
Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression | Q34789045 | ||
Transient outward potassium current, 'Ito', phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms | Q36098638 | ||
Molecular physiology of cardiac repolarization | Q36267771 | ||
Four kinetically distinct depolarization-activated K+ currents in adult mouse ventricular myocytes | Q36420431 | ||
Molecular and metabolic mechanisms of cardiac dysfunction in diabetes. | Q36674142 | ||
Contribution of impaired myocardial insulin signaling to mitochondrial dysfunction and oxidative stress in the heart. | Q37335886 | ||
Role of heteromultimers in the generation of myocardial transient outward K+ currents. | Q38290963 | ||
QTc interval prolongation is a predictor of future strokes in patients with type 2 diabetes mellitus | Q40571031 | ||
Downregulation of K(+) channel genes expression in type I diabetic cardiomyopathy | Q43600224 | ||
Altered K(+) channel gene expression in diabetic rat ventricle: isoform switching between Kv4.2 and Kv1.4. | Q43737948 | ||
Gender-dependent attenuation of cardiac potassium currents in type 2 diabetic db/db mice | Q44705248 | ||
Optical mapping of propagation changes induced by elevated extracellular potassium ion concentration in genetically altered mouse hearts | Q45144975 | ||
Heterogeneous expression of repolarizing, voltage-gated K+ currents in adult mouse ventricles | Q47350584 | ||
Molecular basis of transient outward K+ current diversity in mouse ventricular myocytes. | Q52132199 | ||
Improvement of the metabolic status recovers cardiac potassium channel synthesis in experimental diabetes. | Q54469547 | ||
Effects of insulin on potassium currents of rat ventricular myocytes in streptozotocin diabetes | Q70963683 | ||
Short-term diabetes alters K+ currents in rat ventricular myocytes | Q72314422 | ||
Effects of diabetic cardiomyopathy on regional electrophysiologic characteristics of rat ventricle | Q73443354 | ||
Potassium currents in ventricular myocytes from genetically diabetic rats | Q73847706 | ||
Functional consequences of elimination of i(to,f) and i(to,s): early afterdepolarizations, atrioventricular block, and ventricular arrhythmias in mice lacking Kv1.4 and expressing a dominant-negative Kv4 alpha subunit | Q73964069 | ||
Type I and II models of diabetes produce different modifications of K+ currents in rat heart: role of insulin | Q74367678 | ||
Diabetes mellitus attenuates the repolarization reserve in mammalian heart | Q79444688 | ||
Ionic mechanisms underlying abnormal QT prolongation and the associated arrhythmias in diabetic rabbits: a role of rapid delayed rectifier K+ current | Q80314928 | ||
P433 | issue | 5 | |
P921 | main subject | preproinsulin | Q7240673 |
P304 | page(s) | H747-54 | |
P577 | publication date | 2013-12-27 | |
P1433 | published in | American Journal of Physiology Heart and Circulatory Physiology | Q3193662 |
P1476 | title | The absence of insulin signaling in the heart induces changes in potassium channel expression and ventricular repolarization | |
P478 | volume | 306 |
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Q38465804 | Identification of drug targets related to the induction of ventricular tachyarrhythmia through a systems chemical biology approach |
Q33166935 | Insight into specific pro-arrhythmic triggers in Brugada and early repolarization syndromes: results of long-term follow-up. |
Q91625356 | Insulin Resistance is Associated with Longitudinal Changes of Cardiac Repolarization Heterogeneity in Apparently Healthy Subjects |
Q37439581 | Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice. |
Q28068153 | Molecular and Electrophysiological Mechanisms Underlying Cardiac Arrhythmogenesis in Diabetes Mellitus |
Q46034115 | Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection. |
Q26752678 | New Molecular Insights of Insulin in Diabetic Cardiomyopathy |
Q36714022 | Reduction in Kv Current Enhances the Temporal Dispersion of the Action Potential in Diabetic Myocytes: Insights From a Novel Repolarization Algorithm |
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