Metabolomic analysis of pressure-overloaded and infarcted mouse hearts

Cardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes in individual metabolic pathways have been described, there has been no global assessment of metabolomic changes in hypertrophic and failing...

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Vydáno v:Circulation. Heart failure Ročník 7; číslo 4; s. 634
Hlavní autoři: Sansbury, Brian E, DeMartino, Angelica M, Xie, Zhengzhi, Brooks, Alan C, Brainard, Robert E, Watson, Lewis J, DeFilippis, Andrew P, Cummins, Timothy D, Harbeson, Matthew A, Brittian, Kenneth R, Prabhu, Sumanth D, Bhatnagar, Aruni, Jones, Steven P, Hill, Bradford G
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.07.2014
Témata:
Animals
Cardiomegaly - diagnosis
Cardiomegaly - metabolism
Cardiomegaly - physiopathology
Disease Models, Animal
Echocardiography
Energy Metabolism - physiology
Heart Failure - diagnosis
Heart Failure - metabolism
Heart Failure - physiopathology
Male
Mice
Mice, Inbred C57BL
Myocardial Infarction - diagnosis
Myocardial Infarction - metabolism
Myocardial Infarction - physiopathology
Myocardium - metabolism
Myocardium - pathology
Oxidative Stress
Stroke Volume
Tandem Mass Spectrometry
heart failure
hypertrophy
metabolomics
mitochondria
amino acids
glycolysis
oxidative stress
ISSN:1941-3297, 1941-3297
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Abstract Cardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes in individual metabolic pathways have been described, there has been no global assessment of metabolomic changes in hypertrophic and failing hearts in vivo. Hence, we investigated the impact of pressure overload and infarction on myocardial metabolism. Male C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occlusion (myocardial infarction [MI]). A combination of LC/MS/MS and GC/MS techniques was used to measure 288 metabolites in these hearts. Both transverse aortic constriction and MI were associated with profound changes in myocardial metabolism affecting up to 40% of all metabolites measured. Prominent changes in branched-chain amino acids were observed after 1 week of transverse aortic constriction and 5 days after MI. Changes in branched-chain amino acids after MI were associated with myocardial insulin resistance. Longer duration of transverse aortic constriction and MI led to a decrease in purines, acylcarnitines, fatty acids, and several lysolipid and sphingolipid species but a marked increase in pyrimidines as well as ascorbate, heme, and other indices of oxidative stress. Cardiac remodeling and contractile dysfunction in hypertrophied hearts were associated with large increases in myocardial, but not plasma, levels of the polyamines putrescine and spermidine as well as the collagen breakdown product prolylhydroxyproline. These findings reveal extensive metabolic remodeling common to both hypertrophic and failing hearts that are indicative of extracellular matrix remodeling, insulin resistance and perturbations in amino acid, and lipid and nucleotide metabolism.
AbstractList Cardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes in individual metabolic pathways have been described, there has been no global assessment of metabolomic changes in hypertrophic and failing hearts in vivo. Hence, we investigated the impact of pressure overload and infarction on myocardial metabolism.BACKGROUNDCardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes in individual metabolic pathways have been described, there has been no global assessment of metabolomic changes in hypertrophic and failing hearts in vivo. Hence, we investigated the impact of pressure overload and infarction on myocardial metabolism.Male C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occlusion (myocardial infarction [MI]). A combination of LC/MS/MS and GC/MS techniques was used to measure 288 metabolites in these hearts. Both transverse aortic constriction and MI were associated with profound changes in myocardial metabolism affecting up to 40% of all metabolites measured. Prominent changes in branched-chain amino acids were observed after 1 week of transverse aortic constriction and 5 days after MI. Changes in branched-chain amino acids after MI were associated with myocardial insulin resistance. Longer duration of transverse aortic constriction and MI led to a decrease in purines, acylcarnitines, fatty acids, and several lysolipid and sphingolipid species but a marked increase in pyrimidines as well as ascorbate, heme, and other indices of oxidative stress. Cardiac remodeling and contractile dysfunction in hypertrophied hearts were associated with large increases in myocardial, but not plasma, levels of the polyamines putrescine and spermidine as well as the collagen breakdown product prolylhydroxyproline.METHODS AND RESULTSMale C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occlusion (myocardial infarction [MI]). A combination of LC/MS/MS and GC/MS techniques was used to measure 288 metabolites in these hearts. Both transverse aortic constriction and MI were associated with profound changes in myocardial metabolism affecting up to 40% of all metabolites measured. Prominent changes in branched-chain amino acids were observed after 1 week of transverse aortic constriction and 5 days after MI. Changes in branched-chain amino acids after MI were associated with myocardial insulin resistance. Longer duration of transverse aortic constriction and MI led to a decrease in purines, acylcarnitines, fatty acids, and several lysolipid and sphingolipid species but a marked increase in pyrimidines as well as ascorbate, heme, and other indices of oxidative stress. Cardiac remodeling and contractile dysfunction in hypertrophied hearts were associated with large increases in myocardial, but not plasma, levels of the polyamines putrescine and spermidine as well as the collagen breakdown product prolylhydroxyproline.These findings reveal extensive metabolic remodeling common to both hypertrophic and failing hearts that are indicative of extracellular matrix remodeling, insulin resistance and perturbations in amino acid, and lipid and nucleotide metabolism.CONCLUSIONSThese findings reveal extensive metabolic remodeling common to both hypertrophic and failing hearts that are indicative of extracellular matrix remodeling, insulin resistance and perturbations in amino acid, and lipid and nucleotide metabolism.
Cardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes in individual metabolic pathways have been described, there has been no global assessment of metabolomic changes in hypertrophic and failing hearts in vivo. Hence, we investigated the impact of pressure overload and infarction on myocardial metabolism. Male C57BL/6J mice were subjected to transverse aortic constriction or permanent coronary occlusion (myocardial infarction [MI]). A combination of LC/MS/MS and GC/MS techniques was used to measure 288 metabolites in these hearts. Both transverse aortic constriction and MI were associated with profound changes in myocardial metabolism affecting up to 40% of all metabolites measured. Prominent changes in branched-chain amino acids were observed after 1 week of transverse aortic constriction and 5 days after MI. Changes in branched-chain amino acids after MI were associated with myocardial insulin resistance. Longer duration of transverse aortic constriction and MI led to a decrease in purines, acylcarnitines, fatty acids, and several lysolipid and sphingolipid species but a marked increase in pyrimidines as well as ascorbate, heme, and other indices of oxidative stress. Cardiac remodeling and contractile dysfunction in hypertrophied hearts were associated with large increases in myocardial, but not plasma, levels of the polyamines putrescine and spermidine as well as the collagen breakdown product prolylhydroxyproline. These findings reveal extensive metabolic remodeling common to both hypertrophic and failing hearts that are indicative of extracellular matrix remodeling, insulin resistance and perturbations in amino acid, and lipid and nucleotide metabolism.
Author Sansbury, Brian E
Bhatnagar, Aruni
Harbeson, Matthew A
Xie, Zhengzhi
Brooks, Alan C
Prabhu, Sumanth D
Watson, Lewis J
DeMartino, Angelica M
Brittian, Kenneth R
Hill, Bradford G
Brainard, Robert E
Jones, Steven P
Cummins, Timothy D
DeFilippis, Andrew P
Author_xml – sequence: 1
  givenname: Brian E
  surname: Sansbury
  fullname: Sansbury, Brian E
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 2
  givenname: Angelica M
  surname: DeMartino
  fullname: DeMartino, Angelica M
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 3
  givenname: Zhengzhi
  surname: Xie
  fullname: Xie, Zhengzhi
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 4
  givenname: Alan C
  surname: Brooks
  fullname: Brooks, Alan C
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 5
  givenname: Robert E
  surname: Brainard
  fullname: Brainard, Robert E
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 6
  givenname: Lewis J
  surname: Watson
  fullname: Watson, Lewis J
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 7
  givenname: Andrew P
  surname: DeFilippis
  fullname: DeFilippis, Andrew P
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 8
  givenname: Timothy D
  surname: Cummins
  fullname: Cummins, Timothy D
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 9
  givenname: Matthew A
  surname: Harbeson
  fullname: Harbeson, Matthew A
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 10
  givenname: Kenneth R
  surname: Brittian
  fullname: Brittian, Kenneth R
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 11
  givenname: Sumanth D
  surname: Prabhu
  fullname: Prabhu, Sumanth D
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 12
  givenname: Aruni
  surname: Bhatnagar
  fullname: Bhatnagar, Aruni
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 13
  givenname: Steven P
  surname: Jones
  fullname: Jones, Steven P
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.)
– sequence: 14
  givenname: Bradford G
  surname: Hill
  fullname: Hill, Bradford G
  email: bradford.hill@louisville.edu
  organization: From the Department of Medicine, Institute of Molecular Cardiology, Division of Cardiology (B.E.S., A.M.D.M., Z.X., A.C.B., R.E.B., L.J.W., A.P.D., K.R.B., A.B., S.P.J., B.G.H.), Department of Medicine, Diabetes and Obesity Center (B.E.S., Z.X., A.C.B., T.D.C., M.A.H., K.R.B., A.B., S.P.J., B.G.H.), Department of Biochemistry and Molecular Biology (A.C.B., A.B., B.G.H.), and Department of Physiology and Biophysics (B.E.S., A.M.D., R.E.B., L.J.W., A.B., S.P.J., B.G.H.), University of Louisville, KY; Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, and Birmingham VAMC, AL (S.D.P.); and Department of Medicine, Johns Hopkins University, Baltimore, MD (A.P.D.). bradford.hill@louisville.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24762972$$D View this record in MEDLINE/PubMed
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Keywords heart failure
hypertrophy
metabolomics
mitochondria
amino acids
glycolysis
oxidative stress
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License 2014 American Heart Association, Inc.
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PublicationTitle Circulation. Heart failure
PublicationTitleAlternate Circ Heart Fail
PublicationYear 2014
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References_xml – reference: 14120429 - Am J Physiol. 1964 Feb;206:294-8
– reference: 15271865 - Circ Res. 2004 Jul 23;95(2):135-45
– reference: 19356713 - Cell Metab. 2009 Apr;9(4):311-26
– reference: 2457329 - Am J Physiol. 1988 Aug;255(2 Pt 2):H325-8
– reference: 19213957 - Circ Res. 2009 Mar 27;104(6):805-12
– reference: 11197960 - J Nucl Med. 2001 Jan;42(1):124-9
– reference: 22496159 - Circulation. 2012 May 8;125(18):2222-31
– reference: 8903329 - J Clin Invest. 1996 Nov 1;98(9):2094-9
– reference: 14736546 - Cardiovasc Res. 2004 Feb 1;61(2):297-306
– reference: 23861485 - Circ Heart Fail. 2013 Sep 1;6(5):1039-48
– reference: 20086077 - Physiol Rev. 2010 Jan;90(1):207-58
– reference: 10898742 - Am J Physiol Gastrointest Liver Physiol. 2000 Jul;279(1):G12-9
– reference: 3172988 - Lipids. 1988 Jun;23(6):580-6
– reference: 9195931 - J Biol Chem. 1997 Jun 27;272(26):16281-7
– reference: 20407209 - J Clin Invest. 2010 May;120(5):1506-14
– reference: 23023704 - J Clin Invest. 2012 Nov;122(11):3919-30
– reference: 17311494 - Annu Rev Nutr. 2007;27:19-40
– reference: 17404155 - Circulation. 2007 Apr 17;115(15):2033-41
– reference: 17646594 - Circulation. 2007 Jul 24;116(4):434-48
– reference: 19176603 - Cardiovasc Res. 2009 May 1;82(2):175-83
– reference: 8121298 - Metabolism. 1994 Feb;43(2):174-9
– reference: 15987803 - Physiol Rev. 2005 Jul;85(3):1093-129
– reference: 20176713 - Circ Heart Fail. 2010 May;3(3):420-30
– reference: 15191896 - Am J Physiol Heart Circ Physiol. 2004 Oct;287(4):H1538-43
– reference: 22927473 - Circulation. 2012 Aug 28;126(9):1110-20
– reference: 22408021 - Am J Physiol Heart Circ Physiol. 2012 May 1;302(9):H1795-805
– reference: 17638516 - Pharmacogenomics. 2007 Jul;8(7):863-6
– reference: 18339649 - Cardiovasc Res. 2008 Jul 15;79(2):331-40
– reference: 2147129 - Circ Res. 1990 Dec;67(6):1334-44
– reference: 8067430 - Am J Physiol. 1994 Aug;267(2 Pt 2):H742-50
– reference: 9462605 - Am J Cardiol. 1998 Jan 1;81(1):45-50
– reference: 11934668 - Am J Physiol Endocrinol Metab. 2002 May;282(5):E1039-45
– reference: 3366475 - Hypertension. 1988 May;11(5):416-26
– reference: 22408028 - Am J Physiol Heart Circ Physiol. 2012 May 15;302(10):H2122-30
– reference: 16828794 - J Mol Cell Cardiol. 2006 Aug;41(2):340-9
– reference: 14805850 - Medicine (Baltimore). 1951 Feb;30(1):21-41
– reference: 22332087 - Adv Nutr. 2011 Nov;2(6):445-56
– reference: 20876116 - Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17797-802
– reference: 507189 - Am J Pathol. 1979 Dec;97(3):505-29
– reference: 7869397 - J Mol Cell Cardiol. 1994 Oct;26(10):1371-5
– reference: 11040106 - J Mol Cell Cardiol. 2000 Nov;32(11):2025-34
– reference: 21155767 - Eur J Clin Invest. 2011 May;41(5):527-38
– reference: 4251767 - Jpn Heart J. 1971 Mar;12(2):177-84
– reference: 17045185 - J Card Fail. 2006 Oct;12(8):644-52
– reference: 11988640 - Heart Fail Rev. 2002 Apr;7(2):161-73
– reference: 22896587 - Circ Res. 2012 Oct 12;111(9):1176-89
– reference: 4233124 - J Clin Invest. 1968 Aug;47(8):1787-94
– reference: 20065148 - Hypertension. 2010 Feb;55(2):508-15
– reference: 2934993 - Am J Physiol. 1986 Jan;250(1 Pt 2):H1-6
– reference: 22932257 - Circulation. 2012 Oct 2;126(14):1705-16
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Snippet Cardiac hypertrophy and heart failure are associated with metabolic dysregulation and a state of chronic energy deficiency. Although several disparate changes...
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StartPage 634
SubjectTerms Animals
Cardiomegaly - diagnosis
Cardiomegaly - metabolism
Cardiomegaly - physiopathology
Disease Models, Animal
Echocardiography
Energy Metabolism - physiology
Heart Failure - diagnosis
Heart Failure - metabolism
Heart Failure - physiopathology
Male
Mice
Mice, Inbred C57BL
Myocardial Infarction - diagnosis
Myocardial Infarction - metabolism
Myocardial Infarction - physiopathology
Myocardium - metabolism
Myocardium - pathology
Oxidative Stress
Stroke Volume
Tandem Mass Spectrometry
Title Metabolomic analysis of pressure-overloaded and infarcted mouse hearts
URI https://www.ncbi.nlm.nih.gov/pubmed/24762972
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