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Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure

Haipeng Sun1, Kristine C Olson1, Chen Gao1

  • 1From Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China (H.S., M.Z., Y.L., Y.W.); Division of Molecular Medicine, Departments of Anesthesiology, Medicine, and Physiology, Molecular Biology Institute, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California, Los Angeles (H.S., C.G., Z.W., J.-Y.Y., S.R., C.D.R., H.C., X.X., Y.W.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (K.C.O., C.L.); Case Cardiovascular Research Institute, Harrington Heart and Vascular Institute, Department of Medicine, Case Western Reserve University, Cleveland, OH (D.A.P., D.J., M.K.J.); Division of Cardiology, Department of Medicine (S.S.) and Sarah W. Stedman Nutrition and Metabolism Center, Departments of Medicine and Pharmacology and Cancer Biology (O.I., C.B.N.), and Duke University School of Medicine, Durham, NC; Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas (W.-J.G., N.S.W., R.M.W., D.T.C.); and Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York, NY (P.C.S.). Dr Schulze is now at the Department of Internal Medicine, Division of Cardiology, Angiology, Pneumology and Intensive Medical Care, Friedrich-Schiller-University, Jena, Germany.

Circulation
|April 10, 2016
PubMed
Abstract

Keywords:
amino acidsheart failuremetabolismoxidant stresspathogenesisremodeling

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