J. Buchanan

发表

Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts.

R. Cooksey, E. Abel, S. Boudina, 2004, Diabetes.

Reduced cardiac efficiency and altered substrate metabolism precedes the onset of hyperglycemia and contractile dysfunction in two mouse models of insulin resistance and obesity.

R. Cooksey, E. Abel, S. Litwin, 2005, Endocrinology.

Impaired expression of hematopoietic growth factors: A candidate mechanism for the hematopoietic defect of aging

J. Buchanan, C. A. Peters, C. J. Rasmussen, 1996, Experimental Gerontology.

Captopril normalizes insulin signaling and insulin-regulated substrate metabolism in obese (ob/ob) mouse hearts.

R. Cooksey, E. Abel, J. Buchanan, 2008, Endocrinology.

Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding.

R. Cooksey, E. Abel, S. Boudina, 2009, Cardiovascular research.

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.

Substrate uptake and metabolism are preserved in hypertrophic caveolin-3 knockout hearts.

P. Fortina, M. Lisanti, W. Koch, 2008, American journal of physiology. Heart and circulatory physiology.

Loss of Lipoprotein Lipase-derived Fatty Acids Leads to Increased Cardiac Glucose Metabolism and Heart Dysfunction*

J. D’Armiento, S. Homma, E. Abel, 2006, Journal of Biological Chemistry.

Integrative PGC-1 (cid:1) Deficiency Accelerates the Transition to Heart Failure in Pressure Overload Hypertrophy hypertrophy by preserving glucose metabolism and preventing oxidative stress.

C. Lelliott, E. Abel, A. Vidal-Puig, 2011 .

PGC-1&bgr; Deficiency Accelerates the Transition to Heart Failure in Pressure Overload Hypertrophy

Torsten Doenst, Antonio Vidal-Puig, C. Lelliott, 2011, Circulation research.

Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism

P. Fortina, M. Lisanti, W. Koch, 2008, Cell cycle.

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.

Integrative PGC-1 (cid:1) Deficiency Accelerates the Transition to Heart Failure in Pressure Overload Hypertrophy hypertrophy by preserving glucose metabolism and preventing oxidative stress.

C. Lelliott, G. Medina-Gómez, Curtis D. Olsen, 2011 .