Joseph Tuinei

发表

UCP3 Regulates Cardiac Efficiency and Mitochondrial Coupling in High Fat–Fed Mice but Not in Leptin-Deficient Mice

E. Abel, S. Boudina, Curtis D. Olsen, 2012, Diabetes.

An APPL1-AMPK signaling axis mediates beneficial metabolic effects of adiponectin in the heart.

F. Thong, A. Xu, R. Palanivel, 2010, American journal of physiology. Endocrinology and metabolism.

Genetic loss of insulin receptors worsens cardiac efficiency in diabetes.

B. Weimer, E. Abel, S. Boudina, 2012, Journal of molecular and cellular cardiology.

PPAR g-induced cardiolipotoxicity in mice is ameliorated by PPAR a deficiency despite increases in fatty acid oxidation

G. Shulman, S. Homma, E. Abel, 2018 .

Antioxidant treatment normalizes mitochondrial energetics and myocardial insulin sensitivity independently of changes in systemic metabolic homeostasis in a mouse model of the metabolic syndrome.

E. Abel, Curtis D. Olsen, S. Litwin, 2015, Journal of molecular and cellular cardiology.

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

B. Weimer, E. Abel, B. O’Neill, 2014, Molecular and Cellular Biology.

A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy.

M. Birnbaum, S. Izumo, E. Abel, 2007, Cell metabolism.

Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses.

E. Abel, B. O’Neill, S. Litwin, 2017, American journal of physiology. Heart and circulatory physiology.

Central Leptin Signaling Is Required to Normalize Myocardial Fatty Acid Oxidation Rates in Caloric-Restricted ob/ob Mice

E. Abel, H. Bugger, Crystal L Sloan, 2011, Diabetes.

Breastfeeding, Cellular Immune Activation, and Myocardial Recovery in Peripartum Cardiomyopathy

Mary V. Marks, M. Drazner, G. Felker, 2019, JACC. Basic to translational science.

Abstract 3889: Pyruvate Dehydrogenase Kinase 4 (PDK4) Deficiency Does Not Impair the Cardiac Metabolic or Contractile Response to Pressure Overload Hypertrophy

Robert A. Harris, E. Abel, S. Litwin, 2009 .

Type 1 Diabetic Akita Mouse Hearts Are Insulin Sensitive but Manifest Structurally Abnormal Mitochondria That Remain Coupled Despite Increased Uncoupling Protein 3

Sheldon E. Litwin, E. Dale Abel, E. Abel, 2008, Diabetes.

PPARγ-induced cardiolipotoxicity in mice is ameliorated by PPARα deficiency despite increases in fatty acid oxidation.

G. Shulman, S. Homma, E. Abel, 2010, The Journal of clinical investigation.

Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction

Chae-Myeong Ha, E. Abel, L. Dell’Italia, 2020, Diabetes.

Serum Proteomic Analysis of Peripartum Cardiomyopathy Reveals Distinctive Dysregulation of Inflammatory and Cholesterol Metabolism Pathways.

Deborah L. Wesley, Mary V. Marks, B. Horne, 2023, JACC. Heart failure.

An APPL1-AMPK signaling axis mediates beneficial metabolic effects of adiponectin in the heart.

R. Palanivel, X. Fang, K. Schram, 2010, American journal of physiology. Endocrinology and metabolism.

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

M. McCrory, C. Riehle, J. Buchanan, 2014, Molecular and Cellular Biology.