EVAN ABEL

Summary

Affiliation: University of Utah
Country: USA

Publications

  1. pmc Critical role for thyroid hormone receptor beta2 in the regulation of paraventricular thyrotropin-releasing hormone neurons
    E D Abel
    Division of Endocrinology, Metabolism and Diabetes, University of Utah School of Medicine 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, UT 84112, USA
    J Clin Invest 107:1017-23. 2001
  2. pmc Central leptin signaling is required to normalize myocardial fatty acid oxidation rates in caloric-restricted ob/ob mice
    Crystal Sloan
    Program in Molecular Medicine, University of Utah, Salt Lake City, Utah, USA
    Diabetes 60:1424-34. 2011
  3. pmc Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice
    Heiko Bugger
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Diabetes 58:1986-97. 2009
  4. pmc Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart development and growth
    Yi Zhu
    Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, School of Medicine, University of Utah, Salt Lake City, Utah, United States of America
    PLoS ONE 8:e54221. 2013
  5. pmc Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction
    Renata O Pereira
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, UT
    J Am Heart Assoc 2:e000301. 2013
  6. pmc Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation
    Yi Zhu
    Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 27:172-84. 2013
  7. pmc Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex
    Quan Jiang Zhang
    College of Health, University of Utah, Salt Lake City, Utah, USA
    Diabetes 61:1848-59. 2012
  8. pmc Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, 15 North 2030 East, Bldg 533, Rm 3110B, Salt Lake City, UT 84112, USA
    Cardiovasc Res 90:234-42. 2011
  9. ncbi Myocardial insulin resistance and cardiac complications of diabetes
    E Dale Abel
    Program in Human Molecular Biology and Genetics, and Division of Endocrinology, Metabolism and Diabetes, The University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    Curr Drug Targets Immune Endocr Metabol Disord 5:219-26. 2005
  10. ncbi Regulation of insulin-responsive aminopeptidase expression and targeting in the insulin-responsive vesicle compartment of glucose transporter isoform 4-deficient cardiomyocytes
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 18:2491-501. 2004

Collaborators

Detail Information

Publications48

  1. pmc Critical role for thyroid hormone receptor beta2 in the regulation of paraventricular thyrotropin-releasing hormone neurons
    E D Abel
    Division of Endocrinology, Metabolism and Diabetes, University of Utah School of Medicine 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, UT 84112, USA
    J Clin Invest 107:1017-23. 2001
    ..Thus TR-beta2 is the key TR isoform responsible for T(3)-mediated negative-feedback regulation by hypophysiotropic TRH neurons...
  2. pmc Central leptin signaling is required to normalize myocardial fatty acid oxidation rates in caloric-restricted ob/ob mice
    Crystal Sloan
    Program in Molecular Medicine, University of Utah, Salt Lake City, Utah, USA
    Diabetes 60:1424-34. 2011
    ..This study was designed to determine the contribution of central and peripheral leptin signaling to myocardial metabolism and function in ob/ob and db/db mice in the absence of diabetes and morbid obesity...
  3. pmc Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice
    Heiko Bugger
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Diabetes 58:1986-97. 2009
    ..To elucidate the molecular basis for mitochondrial dysfunction, which has been implicated in the pathogenesis of diabetes complications...
  4. pmc Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart development and growth
    Yi Zhu
    Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, School of Medicine, University of Utah, Salt Lake City, Utah, United States of America
    PLoS ONE 8:e54221. 2013
    ..As a result 92% of embryos with cardiomyocyte Mtor deficiency died by the end of gestation. Thus Mtor is required for survival and proliferation of cardiomyocytes in the developing heart...
  5. pmc Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction
    Renata O Pereira
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, UT
    J Am Heart Assoc 2:e000301. 2013
    ..Therefore, we sought to determine if a short-term increase in GLUT1-mediated myocardial glucose uptake would still confer cardioprotection if overexpression occurred at the onset of POH...
  6. pmc Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation
    Yi Zhu
    Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 27:172-84. 2013
    ..Thus, constitutive activation of PI3K and Akt in cardiomyocytes impairs GLUT4-mediated glucose uptake via mechanisms that impair the function of GLUT4 after its plasma-membrane insertion...
  7. pmc Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex
    Quan Jiang Zhang
    College of Health, University of Utah, Salt Lake City, Utah, USA
    Diabetes 61:1848-59. 2012
    ..These results provide important insight into a pathway that represents a novel target for reversing obesity-related vascular dysfunction...
  8. pmc Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, 15 North 2030 East, Bldg 533, Rm 3110B, Salt Lake City, UT 84112, USA
    Cardiovasc Res 90:234-42. 2011
    ..We suggest that mitochondrial adaptations to pathological and physiological hypertrophy are distinct, and we shall review potential mechanisms that might account for these differences...
  9. ncbi Myocardial insulin resistance and cardiac complications of diabetes
    E Dale Abel
    Program in Human Molecular Biology and Genetics, and Division of Endocrinology, Metabolism and Diabetes, The University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    Curr Drug Targets Immune Endocr Metabol Disord 5:219-26. 2005
    ....
  10. ncbi Regulation of insulin-responsive aminopeptidase expression and targeting in the insulin-responsive vesicle compartment of glucose transporter isoform 4-deficient cardiomyocytes
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 18:2491-501. 2004
    ..Thus, GLUT4 and IRAP content of early endosome-derived sorting vesicles and of IRVs are coordinately regulated, and both proteins are required for maintenance of key constituents of these compartments in cardiac muscle cells in vivo...
  11. ncbi Insulin signaling in heart muscle: lessons from genetically engineered mouse models
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes, University of Utah, 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, UT 84112, USA
    Curr Hypertens Rep 6:416-23. 2004
    ....
  12. ncbi Dominant inhibition of thyroid hormone action selectively in the pituitary of thyroid hormone receptor-beta null mice abolishes the regulation of thyrotropin by thyroid hormone
    E Dale Abel
    Division of Endocrinology, University of Utah School of Medicine, 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 17:1767-76. 2003
    ....
  13. ncbi Glucose transport in the heart
    E Dale Abel
    Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, USA
    Front Biosci 9:201-15. 2004
    ..This review will summarize the current state of knowledge regarding the regulation of glucose transporter expression, and the regulation of glucose transport into myocardial cells...
  14. pmc Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding
    Jordan J Wright
    Division of Endocrinology, Metabolism and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, 15 N 2030 East, Bldg 533, Rm 3110B, Salt Lake City, UT 84112, USA
    Cardiovasc Res 82:351-60. 2009
    ..The study was designed to test the hypothesis that impaired glucose utilization accounts for initial changes in FA metabolism...
  15. pmc Captopril normalizes insulin signaling and insulin-regulated substrate metabolism in obese (ob/ob) mouse hearts
    Imene Tabbi-Anneni
    Division of Endocrinology, Metabolism, and Diabetes, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
    Endocrinology 149:4043-50. 2008
    ..Thus, angiotensin-converting enzyme inhibitors restore the responsiveness of ob/ob mouse hearts to insulin and normalizes AMPK activity independently of effects on systemic metabolic homeostasis...
  16. ncbi Reduced cardiac efficiency and altered substrate metabolism precedes the onset of hyperglycemia and contractile dysfunction in two mouse models of insulin resistance and obesity
    Jonathan Buchanan
    Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, 84112, USA
    Endocrinology 146:5341-9. 2005
    ....
  17. ncbi Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts
    Pradip K Mazumder
    Program in Human Molecular Biology and Genetics, Division of Endocrinology, Metabolism and Diabetes, University of Utah, 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, UT 84112, USA
    Diabetes 53:2366-74. 2004
    ....
  18. ncbi Mouse and human resistins impair glucose transport in primary mouse cardiomyocytes, and oligomerization is required for this biological action
    Christophe Graveleau
    Division of Endocrinology, Metabolism, and Diabetes, University of Utah, Salt Lake City, Utah 84112, USA
    J Biol Chem 280:31679-85. 2005
    ..Thus, in cardiomyocytes, both mouse and human resistins directly impair glucose transport; and in contrast to effects on the liver, these actions of resistin require oligomerization...
  19. pmc Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice
    Adam R Wende
    Program in Molecular Medicine and Division of Endocrinology, Metabolism, and Diabetes, University of Utah, School of Medicine, Salt Lake City, Utah 84112, USA
    Endocrinology 151:3536-42. 2010
    ..In conclusion, complete loss of bradykinin expression does not worsen cardiac function or increase myocardial fibrosis in diabetes...
  20. pmc Endothelial nitric oxide synthase phosphorylation in treadmill-running mice: role of vascular signalling kinases
    Quan Jiang Zhang
    College of Health, University of Utah, Salt Lake City, UT 84132, USA
    J Physiol 587:3911-20. 2009
    ..These findings indicate that Akt and AMPK contribute importantly to vascular eNOS S1177 phosphorylation during treadmill-running, and that AMPK is sufficient to activate p-eNOS S1177 in the presence of PI3K inhibition...
  21. pmc Contribution of impaired myocardial insulin signaling to mitochondrial dysfunction and oxidative stress in the heart
    Sihem Boudina
    University of Utah School of Medicine, Salt Lake City, 84112, USA
    Circulation 119:1272-83. 2009
    ..The present study tested the hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondrial function...
  22. ncbi Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload
    Ping Hu
    Division of Cardiology, University Hospital, The University of Utah, 50 N Medical Drive, Salt Lake City, UT 84132, USA
    Am J Physiol Heart Circ Physiol 285:H1261-9. 2003
    ..The use of the MTAB approach should facilitate the study of the pathophysiology and treatment of pressure-overload hypertrophy...
  23. ncbi Cardiac hypertrophy caused by peroxisome proliferator- activated receptor-gamma agonist treatment occurs independently of changes in myocardial insulin signaling
    Sandra Sena
    Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, 15 North 2030 East, Salt Lake City, UT 84112, USA
    Endocrinology 148:6047-53. 2007
    ..These data indicate that cardiac hypertrophy after PPAR-gamma agonist treatment can occur in the absence of myocardial insulin signaling and is likely secondary to the hemodynamic consequences of plasma volume expansion...
  24. pmc Contribution of insulin and Akt1 signaling to endothelial nitric oxide synthase in the regulation of endothelial function and blood pressure
    J David Symons
    College of Health, University of Utah School of Medicine, 30 N 2030 E, Salt Lake City, UT 84132, USA
    Circ Res 104:1085-94. 2009
    ....
  25. pmc Dietary iron restriction or iron chelation protects from diabetes and loss of beta-cell function in the obese (ob/ob lep-/-) mouse
    Robert C Cooksey
    Department of Medicine, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
    Am J Physiol Endocrinol Metab 298:E1236-43. 2010
    ..We conclude that, even at "normal" levels, iron exerts detrimental effects on beta-cell function that are reversible with dietary restriction or pharmacotherapy...
  26. ncbi Optical mapping of propagation changes induced by elevated extracellular potassium ion concentration in genetically altered mouse hearts
    Bonnie B Punske
    Nora Eccles Harrison Cardiovascular Research and Training Institute, The University of Utah, Salt Lake City, UT 84112 5000, USA
    J Electrocardiol 37:128-34. 2004
    ..This study employed optical mapping to characterize propagation changes in intact mouse hearts with cardiomyocyte-restricted knock out of insulin receptors (CIRKO)...
  27. pmc Aberrant water homeostasis detected by stable isotope analysis
    Shannon P O'Grady
    Department of Biology, University of Utah, Salt Lake City, Utah, United States of America
    PLoS ONE 5:e11699. 2010
    ....
  28. pmc 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
    Jingyu Huang
    Departments of Medicine and Biochemistry, University of Utah School of Medicine, Salt Lake City, USA
    Diabetes 60:80-7. 2011
    ..This effect by itself is not sufficient, however, to fully explain the diabetes risk phenotype associated with all forms of iron overload...
  29. pmc CRYAB and HSPB2 deficiency alters cardiac metabolism and paradoxically confers protection against myocardial ischemia in aging mice
    Ivor J Benjamin
    Center for Cardiovascular Translational Biomedicine, University of Utah, School of Medicine, Salt Lake City, UT, USA
    Am J Physiol Heart Circ Physiol 293:H3201-9. 2007
    ..We discuss the implications of these disparate results in the context of phenotypic responses reported for CRYAB/HSPB2-deficient mice to different ischemic challenges...
  30. pmc Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload
    J David Symons
    College of Health, and Univ of Utah School of Medicine, Bldg 585, Rm 168, 30 N 2030 E Salt Lake City, UT 84132, USA
    Am J Physiol Heart Circ Physiol 300:H374-81. 2011
    ..g., increased eNOS transcript and protein) to maintain coronary endothelial function in the setting of pressure overload...
  31. pmc Lipotoxicity in the heart
    Adam R Wende
    Program in Molecular Medicine and Division of Endocrinology, Metabolism, and Diabetes, University of Utah, School of Medicine, Salt Lake City, UT 84112, USA
    Biochim Biophys Acta 1801:311-9. 2010
    ..We will seek to highlight those areas where additional research is warranted...
  32. pmc Iron-mediated inhibition of mitochondrial manganese uptake mediates mitochondrial dysfunction in a mouse model of hemochromatosis
    Hani A Jouihan
    Department of Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Mol Med 14:98-108. 2008
    ..These data suggest a novel mechanism of iron-induced cellular dysfunction, namely altered mitochondrial uptake of other metal ions...
  33. ncbi Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes
    Sihem Boudina
    Division of Endocrinology, Metabolism, and Diabetes, and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Physiology (Bethesda) 21:250-8. 2006
    ..Here, we review possible mechanisms for reduced cardiac efficiency in obesity and diabetes by focusing on the potential role of mitochondrial uncoupling...
  34. pmc PAS kinase is required for normal cellular energy balance
    Huai Xiang Hao
    Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    Proc Natl Acad Sci U S A 104:15466-71. 2007
    ..We therefore hypothesize that PASK acts in a cell-autonomous manner to maintain cellular energy homeostasis and is a potential therapeutic target for metabolic disease...
  35. pmc Insulin-like growth factor I receptor signaling is required for exercise-induced cardiac hypertrophy
    Jaetaek Kim
    Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah 84112, USA
    Mol Endocrinol 22:2531-43. 2008
    ..These signaling events antagonize Akt signaling, which although necessary for mediating physiological cardiac hypertrophy, is insufficient to promote cardiac hypertrophy in the absence of myocardial IGF-I signaling...
  36. pmc Akt1 in the cardiovascular system: friend or foe?
    Brian T O'Neill
    Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
    J Clin Invest 115:2059-64. 2005
    ..Here we discuss the implications of these exciting new studies...
  37. ncbi Recipes for creating animal models of diabetic cardiovascular disease
    Willa Hsueh
    Division of Endocrinology, Diabetes, and Hypertension, The David Geffen School of Medicine, University of California, Los Angeles, CA, USA
    Circ Res 100:1415-27. 2007
    ....
  38. ncbi Reduced mitochondrial oxidative capacity and increased mitochondrial uncoupling impair myocardial energetics in obesity
    Sihem Boudina
    Division of Endocrinology, Metabolism and Diabetes, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Circulation 112:2686-95. 2005
    ..The present study was performed to determine whether mitochondrial dysfunction and uncoupling are responsible for reduced cardiac performance and efficiency in ob/ob mice...
  39. ncbi Diabetic cardiomyopathy revisited
    Sihem Boudina
    Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City 84112, USA
    Circulation 115:3213-23. 2007
    ..This review discusses the latest findings in diabetic humans and in animal models and reviews emerging new mechanisms that may be involved in the development and progression of cardiac dysfunction in diabetes...
  40. pmc Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3
    Heiko Bugger
    Division of Endocrinology, Metabolism, and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Diabetes 57:2924-32. 2008
    ..We hypothesized that mitochondrial uncoupling may also contribute to reduced cardiac efficiency and contractile dysfunction in the type 1 diabetic Akita mouse model (Akita)...
  41. doi Rodent models of diabetic cardiomyopathy
    Heiko Bugger
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
    Dis Model Mech 2:454-66. 2009
    ....
  42. doi Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome
    Heiko Bugger
    Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    Clin Sci (Lond) 114:195-210. 2008
    ..This review will discuss potential molecular mechanisms for these mitochondrial abnormalities...
  43. doi Reversal of oxidative stress in endothelial cells by controlled release of adiponectin
    Mohanad Mossalam
    Department of Pharmaceutics and Pharmaceutical Chemistry, Center for Controlled Chemical Delivery, University of Utah, Salt Lake City, UT 84112, USA
    J Control Release 130:234-7. 2008
    ..These data provide a rationale for developing controlled release dosage form of gAdp as a therapeutic tool for oxidative stress-related pathology in patients with diabetes...
  44. pmc Impaired insulin signaling accelerates cardiac mitochondrial dysfunction after myocardial infarction
    Sandra Sena
    Division of Endocrinology Metabolism and Diabetes, Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    J Mol Cell Cardiol 46:910-8. 2009
    ....
  45. pmc PGC-1β deficiency accelerates the transition to heart failure in pressure overload hypertrophy
    Christian Riehle
    Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
    Circ Res 109:783-93. 2011
    ....
  46. pmc A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy
    Brian T O'Neill
    Program in Human Molecular Biology and Genetics and Division of Endocrinology, Metabolism, and Diabetes, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
    Cell Metab 6:294-306. 2007
    ..Although PI3K signaling to Akt1 is required for cellular growth, Akt-independent pathways mediate the accompanying mitochondrial adaptations...
  47. ncbi Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins
    Sihem Boudina
    Division of Endocrinology, Metabolism, and Diabetes, Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA
    Diabetes 56:2457-66. 2007
    ..Mitochondrial uncoupling has been proposed to contribute to these metabolic abnormalities but has not been directly demonstrated...
  48. pmc Mammalian target of rapamycin is a critical regulator of cardiac hypertrophy in spontaneously hypertensive rats
    Will Soesanto
    College of Health, University of Utah, Salt Lake City, UT 84112, USA
    Hypertension 54:1321-7. 2009
    ..These data show that mammalian target of rapamycin is required for the development of cardiac hypertrophy evoked by rising blood pressure in SHRs...

Research Grants16

  1. Insulin Signaling and the Heart in Diabetes
    EVAN DALE ABEL; Fiscal Year: 2010
    ..Moreover, elucidation of the signaling mechanisms that regulate autophagy in cardiomyocytes may lead to novel therapies for preventing or modulating heart injury as occurs in diabetes, cardiac ischemia or cardiac hypertrophy. ..
  2. Insulin resistance and cardiac dysfunction in obesity
    EVAN ABEL; Fiscal Year: 2007
    ..These studies will provide a detailed and comprehensive analysis of the role that abnormal myocardial insulin signaling plays in the pathogenesis of cardiac dysfunction in obesity. ..
  3. Insulin resistance and cardiac dysfunction in obesity
    EVAN ABEL; Fiscal Year: 2003
    ..These studies will provide a detailed and comprehensive analysis of the role that abnormal myocardial insulin signaling plays in the pathogenesis of cardiac dysfunction in obesity. ..
  4. Modeling Diabetic Cardiomyopathy and Microangiopathy
    EVAN ABEL; Fiscal Year: 2007
    ....
  5. Insulin Signaling and the Heart in Diabetes
    EVAN ABEL; Fiscal Year: 2007
    ..These studies will shed important insight into the regulation of cardiac function and metabolism by insulin and the role of impaired insulin signaling in the pathogenesis of diabetic cardiomyopathy. ..
  6. Targeting Antioxidant Therapy to Cardiac Mitochondria
    EVAN ABEL; Fiscal Year: 2006
    ..Once efficacy is determined, promising reagents can then be subjected to pharmacokinetic and toxicological analysis following systemic administration. ..
  7. Insulin Signaling and the Heart in Diabetes
    EVAN ABEL; Fiscal Year: 2005
    ..These studies will shed important insight into the regulation of cardiac function and metabolism by insulin and the role of impaired insulin signaling in the pathogenesis of diabetic cardiomyopathy. ..
  8. Insulin resistance and cardiac dysfunction in obesity
    EVAN ABEL; Fiscal Year: 2006
    ..These studies will provide a detailed and comprehensive analysis of the role that abnormal myocardial insulin signaling plays in the pathogenesis of cardiac dysfunction in obesity. ..
  9. Insulin Signaling and the Heart in Diabetes
    EVAN ABEL; Fiscal Year: 2006
    ..These studies will shed important insight into the regulation of cardiac function and metabolism by insulin and the role of impaired insulin signaling in the pathogenesis of diabetic cardiomyopathy. ..
  10. Insulin resistance and cardiac dysfunction in obesity
    EVAN ABEL; Fiscal Year: 2005
    ..These studies will provide a detailed and comprehensive analysis of the role that abnormal myocardial insulin signaling plays in the pathogenesis of cardiac dysfunction in obesity. ..
  11. Insulin Signaling and the Heart in Diabetes
    EVAN ABEL; Fiscal Year: 2005
    ..These studies will shed important insight into the regulation of cardiac function and metabolism by insulin and the role of impaired insulin signaling in the pathogenesis of diabetic cardiomyopathy. ..
  12. Insulin resistance and cardiac dysfunction in obesity
    EVAN ABEL; Fiscal Year: 2004
    ..These studies will provide a detailed and comprehensive analysis of the role that abnormal myocardial insulin signaling plays in the pathogenesis of cardiac dysfunction in obesity. ..
  13. Insulin Signaling and the Heart in Diabetes
    EVAN ABEL; Fiscal Year: 2004
    ..These studies will shed important insight into the regulation of cardiac function and metabolism by insulin and the role of impaired insulin signaling in the pathogenesis of diabetic cardiomyopathy. ..