E. Dale Abel American endocrinologist
Abel, E.D.
Abel, E. D. (E. Dale)
Abel, Evan D.
VIAF ID: 62604676 (Personal)
Permalink: http://viaf.org/viaf/62604676
Preferred Forms
- 100 1 _ ‡a Abel, E. D. ‡q (E. Dale)
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- 100 1 _ ‡a Abel, E.D.
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- 100 1 _ ‡a Abel, Evan D.
- 100 0 _ ‡a E. Dale Abel ‡c American endocrinologist
4xx's: Alternate Name Forms (6)
Works
Title | Sources |
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Cardiovascular pharmacogenetics, c2004: | |
Glucose metabolism is linked to the inflammatory status of macrophages. | |
Glucose Metabolism Is Required for Platelet Hyperactivation in a Murine Model of Type 1 Diabetes | |
Glucose transporter 1-mediated glucose uptake is limiting for B-cell acute lymphoblastic leukemia anabolic metabolism and resistance to apoptosis. | |
Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses. | |
The glucose transporter GLUT1 is required for ErbB2-induced mammary tumorigenesis | |
The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function | |
GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure. | |
Handbuch der experimentellen Pharmakologie | |
Heart Failure in Type 2 Diabetes Mellitus | |
Heart-specific ablation of Prkar1a causes failure of heart development and myxomagenesis | |
Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism | |
Impaired transcriptional activity of Nrf2 in age-related myocardial oxidative stress is reversible by moderate exercise training. | |
Increased glycolysis mediates Wnt7b-induced bone formation | |
Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction. | |
Inefficient reprogramming of fibroblasts into cardiomyocytes using Gata4, Mef2c, and Tbx5 | |
Inhibiting Insulin-Mediated β2-Adrenergic Receptor Activation Prevents Diabetes-Associated Cardiac Dysfunction. | |
Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart. | |
Insulin and IGF-1 receptors regulate FoxO-mediated signaling in muscle proteostasis. | |
Insulin-dependent metabolic and inotropic responses in the heart are modulated by hydrogen peroxide from NADPH-oxidase isoforms NOX2 and NOX4. | |
Insulin inhibits cardiac contractility by inducing a Gi-biased β2-adrenergic signaling in hearts. | |
Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training. | |
Insulin regulation of myocardial autophagy. | |
Insulin signaling in heart muscle: lessons from genetically engineered mouse models. | |
Insulin stimulates mitochondrial fusion and function in cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 signaling pathway | |
Insulin suppresses ischemic preconditioning-mediated cardioprotection through Akt-dependent mechanisms. | |
Iron-mediated inhibition of mitochondrial manganese uptake mediates mitochondrial dysfunction in a mouse model of hemochromatosis. | |
Iron overload and diabetes risk: a shift from glucose to Fatty Acid oxidation and increased hepatic glucose production in a mouse model of hereditary hemochromatosis. | |
Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload | |
Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis. | |
Lipids, lysosomes, and autophagy. | |
Lipotoxicity contributes to endothelial dysfunction: a focus on the contribution from ceramide. | |
Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice. | |
Loss of lipoprotein lipase-derived fatty acids leads to increased cardiac glucose metabolism and heart dysfunction. | |
Loss of MCU prevents mitochondrial fusion in G1-S phase and blocks cell cycle progression and proliferation | |
Lysosomal reacidification by degradation of poly(dl-lactide-CO-glycolide) nanoparticles in a lipotoxic cardiomyopathy model, December 2016: | |
Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function. | |
Mammalian target of rapamycin is a critical regulator of cardiac hypertrophy in spontaneously hypertensive rats. | |
The maximal downstroke of epicardial potentials as an index of electrical activity in mouse hearts | |
Mechanisms of leucocyte sodium influx in essential hypertension | |
Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart development and growth | |
Mice expressing human but not murine beta3-adrenergic receptors under the control of human gene regulatory elements. | |
Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload | |
Mitochondrial Calpain-1 Disrupts ATP Synthase and Induces Superoxide Generation in Type 1 Diabetic Hearts: A Novel Mechanism Contributing to Diabetic Cardiomyopathy | |
MITOCHONDRIAL DYNAMICS AND METABOLIC REGULATION IN CARDIAC AND SKELETAL MUSCLE | |
Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins. | |
Mitochondrial fusion and function in Charcot-Marie-Tooth type 2A patient fibroblasts with mitofusin 2 mutations | |
Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induces Post-Translational Modifications of AKAP121, DRP1 and OPA1 That Promote Mitochondrial Fission. | |
Modulating GLUT1 expression in retinal pigment epithelium decreases glucose levels in the retina: impact on photoreceptors and Müller glial cells | |
Modulation of glucose transporter 1 (GLUT1) expression levels alters mouse mammary tumor cell growth in vitro and in vivo. | |
Modulation of the cardiovascular system by leptin. | |
Mouse and human resistins impair glucose transport in primary mouse cardiomyocytes, and oligomerization is required for this biological action. | |
Myeloid -Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1 | |
Myocardial mitochondrial dysfunction in mice lacking adiponectin receptor 1. | |
A new twist in the function of the cardiac lipid droplet | |
Nicotinamide riboside is uniquely and orally bioavailable in mice and humans | |
Nox4 reprograms cardiac substrate metabolism via protein O-GlcNAcylation to enhance stress adaptation. | |
Nrf2 deficiency prevents reductive stress-induced hypertrophic cardiomyopathy. | |
Nuclear receptor SHP, a death receptor that targets mitochondria, induces apoptosis and inhibits tumor growth. | |
Obesity stresses cardiac mitochondria even when you are young | |
OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance. | |
p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas | |
PAS kinase is required for normal cellular energy balance | |
PGC-1 proteins and heart failure | |
Phosphoenolpyruvate Is a Metabolic Checkpoint of Anti-tumor T Cell Responses. | |
Phosphoinositide dependent protein kinase 1 is required for exercise-induced cardiac hypertrophy but not the associated mitochondrial adaptations | |
Podocyte-specific GLUT4-deficient mice have fewer and larger podocytes and are protected from diabetic nephropathy. | |
PPARγ-induced cardiolipotoxicity in mice is ameliorated by PPARα deficiency despite increases in fatty acid oxidation. | |
Prorenin independently causes hypertension and renal and cardiac fibrosis in cyp1a1-prorenin transgenic rats. | |
Publisher Correction: Mitochondrial pyruvate carriers are required for myocardial stress adaptation | |
Reduced cardiac efficiency and altered substrate metabolism precedes the onset of hyperglycemia and contractile dysfunction in two mouse models of insulin resistance and obesity. | |
Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1α | |
Regulation of insulin-responsive aminopeptidase expression and targeting in the insulin-responsive vesicle compartment of glucose transporter isoform 4-deficient cardiomyocytes. | |
Rodent models of diabetic cardiomyopathy. | |
The role of mPer2 clock gene in glucocorticoid and feeding rhythms. | |
Spotlight on metabolic remodelling in heart failure | |
Substrate uptake and metabolism are preserved in hypertrophic caveolin-3 knockout hearts | |
Superoxide Dismutase 2 is dispensable for platelet function. | |
SWELL1 regulates skeletal muscle cell size, intracellular signalling, adiposity and glucose metabolism | |
Systematic Transmission Electron Microscopy‐Based Identification and 3D Reconstruction of Cellular Degradation Machinery | |
Talin1 has unique expression versus talin 2 in the heart and modifies the hypertrophic response to pressure overload. | |
Targeted deletion of BMK1/ERK5 in adult mice perturbs vascular integrity and leads to endothelial failure. | |
Targeting myocardial substrate metabolism in heart failure: potential for new therapies | |
Thyrocyte-specific deletion of insulin and IGF-1 receptors induces papillary thyroid carcinoma-like lesions through EGFR pathway activation | |
Time to Look Back and to Look Forward | |
Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice. | |
Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3. | |
UCP3 regulates cardiac efficiency and mitochondrial coupling in high fat-fed mice but not in leptin-deficient mice. | |
An unliganded thyroid hormone receptor causes severe neurological dysfunction |