E Dale Abel

Summary

Affiliation: University of Iowa
Country: USA

Publications

  1. Fidler T, Marti A, Gerth K, Middleton E, Campbell R, Rondina M, et al. Glucose Metabolism Is Required for Platelet Hyperactivation in a Murine Model of Type 1 Diabetes. Diabetes. 2019;68:932-938 pubmed publisher
    ..These data reveal that increased platelet glucose metabolism in vivo contributes to increased platelet activation and thrombosis in a model of T1DM. ..
  2. Ilkun O, Wilde N, Tuinei J, Pires K, Zhu Y, Bugger H, et al. Antioxidant treatment normalizes mitochondrial energetics and myocardial insulin sensitivity independently of changes in systemic metabolic homeostasis in a mouse model of the metabolic syndrome. J Mol Cell Cardiol. 2015;85:104-16 pubmed publisher
    ..Pharmacological ROS scavenging improves myocardial energy metabolism and insulin responsiveness in obesity and type 2 diabetes via direct effects that might be independent of changes in systemic metabolism. ..
  3. Pereira R, Wende A, Crum A, Hunter D, Olsen C, Rawlings T, et al. Maintaining PGC-1? expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function. FASEB J. 2014;28:3691-702 pubmed publisher
    ..Hence, sustaining physiological levels of PGC-1? expression following POH, while preserving myocardial vascularity, does not prevent mitochondrial and contractile dysfunction. ..
  4. Noh J, Wende A, Olsen C, Kim B, Bevins J, Zhu Y, et al. Phosphoinositide dependent protein kinase 1 is required for exercise-induced cardiac hypertrophy but not the associated mitochondrial adaptations. J Mol Cell Cardiol. 2015;89:297-305 pubmed publisher
    ..1±0.9, P=0.04; cPDPK1(+/-): 12.4±0.6 vs.15.9±1.2, P=0.04). These findings suggest that PDPK1 is required for exercise-induced cardiac hypertrophy but does not contribute to exercise-induced increases in mitochondrial function. ..
  5. Ock S, Lee W, Kim H, Park K, Kim Y, Kook H, et al. Connexin43 and zonula occludens-1 are targets of Akt in cardiomyocytes that correlate with cardiac contractile dysfunction in Akt deficient hearts. Biochim Biophys Acta Mol Basis Dis. 2018;1864:1183-1191 pubmed publisher
    ..Loss of Akt signaling disrupts gap junction protein, which might precipitate early contractile dysfunction prior to heart failure in the absence of myocardial remodeling, such as hypertrophy, fibrosis, or cell death. ..
  6. Wende A, O Neill B, Bugger H, Riehle C, Tuinei J, Buchanan J, et al. Enhanced cardiac Akt/protein kinase B signaling contributes to pathological cardiac hypertrophy in part by impairing mitochondrial function via transcriptional repression of mitochondrion-targeted nuclear genes. Mol Cell Biol. 2015;35:831-46 pubmed publisher
  7. Jaishy B, Abel E. Lipids, lysosomes, and autophagy. J Lipid Res. 2016;57:1619-35 pubmed publisher
  8. Pereira R, Tadinada S, Zasadny F, Oliveira K, Pires K, Olvera A, et al. OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance. EMBO J. 2017;36:2126-2145 pubmed publisher
    ..OPA1-elicited mitochondrial dysfunction activates an integrated stress response that locally induces muscle atrophy, but via secretion of FGF21 acts distally to modulate whole-body metabolism. ..
  9. Fidler T, Middleton E, Rowley J, Boudreau L, Campbell R, Souvenir R, et al. Glucose Transporter 3 Potentiates Degranulation and Is Required for Platelet Activation. Arterioscler Thromb Vasc Biol. 2017;37:1628-1639 pubmed publisher
    ..GLUT3-mediated glucose utilization and glycogenolysis in platelets promotes ?-granule release, platelet activation, and postactivation functions. ..

More Information

Publications12

  1. Fidler T, Rowley J, Araújo C, Boudreau L, Marti A, Souvenir R, et al. Superoxide Dismutase 2 is dispensable for platelet function. Thromb Haemost. 2017;117:1859-1867 pubmed publisher
    ..These data demonstrate that increased mitochondrial ROS does not result in platelet dysfunction. ..
  2. Tsushima K, Bugger H, Wende A, Soto J, Jenson G, Tor A, et al. Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission. Circ Res. 2018;122:58-73 pubmed publisher
    ..These findings provide a novel mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy. ..
  3. Fidler T, Campbell R, Funari T, Dunne N, Balderas Angeles E, Middleton E, et al. Deletion of GLUT1 and GLUT3 Reveals Multiple Roles for Glucose Metabolism in Platelet and Megakaryocyte Function. Cell Rep. 2017;20:881-894 pubmed publisher
    ..Thus, substrate metabolism is essential for platelet production, activation, and survival. ..