Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction - Wikidata - wikimedia - TriplyDB

Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction

Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction

http://www.wikidata.org/entity/Q35739201

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Altered lipid metabolism in residual white adipose tissues of Bscl2 deficient mice Multiphasic triacylglycerol dynamics in the intact heart during acute in vivo overexpression of CD36 Sestrin 1 ameliorates cardiac hypertrophy via autophagy activation.Deficiency of a lipid droplet protein, perilipin 5, suppresses myocardial lipid accumulation, thereby preventing type 1 diabetes-induced heart malfunction Cardiac steatosis potentiates angiotensin II effects in the heart.PEDF and PEDF-derived peptide 44mer stimulate cardiac triglyceride degradation via ATGL.Enhancing Cardiac Triacylglycerol Metabolism Improves Recovery From Ischemic Stress.AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism.Adipose Tissue Lipolysis Promotes Exercise-induced Cardiac Hypertrophy Involving the Lipokine C16:1n7-Palmitoleate.Mechanisms of lipotoxicity in the cardiovascular system.Comparative proteomics reveals abnormal binding of ATGL and dysferlin on lipid droplets from pressure overload-induced dysfunctional rat hearts Cardiac-specific overexpression of perilipin 5 provokes severe cardiac steatosis via the formation of a lipolytic barrier.Aldose Reductase Acts as a Selective Derepressor of PPARγ and the Retinoic Acid Receptor.Normalization of cardiac substrate utilization and left ventricular hypertrophy precede functional recovery in heart failure regression.Cardiac lipotoxicity: molecular pathways and therapeutic implications.Early structural and metabolic cardiac remodelling in response to inducible adipose triglyceride lipase ablation.Skeletal muscle triacylglycerol hydrolysis does not influence metabolic complications of obesity.Cardiac oxidative stress in a mouse model of neutral lipid storage disease.Lipid Use and Misuse by the Heart.Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes.Matrix revisited: mechanisms linking energy substrate metabolism to the function of the heart.Good and bad consequences of altered fatty acid metabolism in heart failure: evidence from mouse models.Hearts lacking plasma membrane KATP channels display changes in basal aerobic metabolic substrate preference and AMPK activity.A novel complex I inhibitor protects against hypertension-induced left ventricular hypertrophy.G0/G1 Switch Gene 2 Regulates Cardiac Lipolysis.Atgl deficiency induces podocyte apoptosis and leads to glomerular filtration barrier damage.Cardiomyocyte-specific ablation of CD36 accelerates the progression from compensated cardiac hypertrophy to heart failure.Metabolism in cardiomyopathy: every substrate matters.Metabolic remodelling in hypertrophied and failing myocardium: a review.Expression of lipogenic genes is upregulated in the heart with exercise training-induced but not pressure overload-induced left ventricular hypertrophy.Myocardial adipose triglyceride lipase overexpression protects diabetic mice from the development of lipotoxic cardiomyopathy.Savings precede spending: fatty acid utilization relies on triglyceride formation for cardiac energetics.Cardiac-specific adipose triglyceride lipase overexpression protects from cardiac steatosis and dilated cardiomyopathy following diet-induced obesity.Cardiomyocyte specific adipose triglyceride lipase overexpression prevents doxorubicin induced cardiac dysfunction in female mice.Infarct-remodelled hearts with limited oxidative capacity boost fatty acid oxidation after conditioning against ischaemia/reperfusion injury.Adipose tissue ATGL modifies the cardiac lipidome in pressure-overload-induced left ventricular failure.Diabetic db/db mice do not develop heart failure upon pressure overload: a longitudinal in vivo PET, MRI, and MRS study on cardiac metabolic, structural, and functional adaptations.Co-administration of resveratrol with doxorubicin in young mice attenuates detrimental late-occurring cardiovascular changes.The Role of Diacylglycerol Acyltransferase (DGAT) 1 and 2 in Cardiac Metabolism and Function.

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Myocardial ATGL overexpression decreases the reliance on fatty acid oxidation and protects against pressure overload-induced cardiac dysfunction

http://www.wikidata.org/entity/Q35739201

description

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Molecular and Cellular Biology

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Myocardial ATGL overexpression ...... ad-induced cardiac dysfunction

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Erin E Kershaw

http://www.w3.org/2001/XMLSchema#string

Gavin Y Oudit

http://www.w3.org/2001/XMLSchema#string

Jason R B Dyck

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Jeevan Nagendran

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Martin E Young

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Miranda M Y Sung

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Peter E Light

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A simple method for the isolation and purification of total lipides from animal tissues

Loss of PI3Kγ enhances cAMP-dependent MMP remodeling of the myocardial N-cadherin adhesion complexes and extracellular matrix in response to early biomechanical stress

High-fat-diet-induced obesity and heart dysfunction are regulated by the TOR pathway in Drosophila

Hyperleptinemia prevents lipotoxic cardiomyopathy in acyl CoA synthase transgenic mice.

Overexpression of the Na+/H+ exchanger and ischemia-reperfusion injury in the myocardium.

Isolation and characterization of the mouse cardiac myosin heavy chain genes.

Direct regulation of myocardial triglyceride metabolism by the cardiomyocyte circadian clock.

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

Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase.

Phospholipid homeostasis regulates lipid metabolism and cardiac function through SREBP signaling in Drosophila

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10.1128/MCB.06470-11

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4

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32

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Guenter Haemmerle

Thomas Pulinilkunnil

Petra C Kienesberger

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2011-12-12T00:00:00Z

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22158969

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3272983

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