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Cardiac Energy Metabolism in Heart Failure

Circulation research, 2021-05, Vol.128 (10), p.1487-1513

2021

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O-GlcNAcylation and cardiovascular disease

Biochemical Society transactions, 2017-04, Vol.45 (2), p.545-553

2017

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Metabolic Origins of Heart Failure

JACC. Basic to translational science, 2017-06, Vol.2 (3), p.297-310

2017

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Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction

Diabetes (New York, N.Y.), 2020-10, Vol.69 (10), p.2094-2111

2020

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Role of O -Linked N -Acetylglucosamine Protein Modification in Cellular (Patho)Physiology

Physiological reviews, 2021-04, Vol.101 (2), p.427-493

2021

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Editorial: Metabolic Regulation of Cardiac and Vascular Cell Function: Physiological and Pathophysiological Implications

Frontiers in physiology, 2022-02, Vol.13, p.849869-849869

2022

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Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice

Redox biology, 2019-02, Vol.21, p.101100-101100, Article 101100

2019

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Cardiomyocyte-Specific BMAL1 Plays Critical Roles in Metabolism, Signaling, and Maintenance of Contractile Function of the Heart

Journal of biological rhythms, 2014-08, Vol.29 (4), p.257-276

2014

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Redox biology and the interface between bioenergetics, autophagy and circadian control of metabolism

Free radical biology & medicine, 2016-11, Vol.100, p.94-107

2016

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Mechanisms of Lipotoxicity in the Cardiovascular System

Current hypertension reports, 2012-12, Vol.14 (6), p.517-531

2012

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

American journal of physiology. Heart and circulatory physiology, 2017-12, Vol.313 (6), p.H1098-H1108

2017

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Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stress

Scientific reports, 2021-06, Vol.11 (1), p.11977-11977, Article 11977

2021

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Insulin Receptor Substrates Are Essential for the Bioenergetic and Hypertrophic Response of the Heart to Exercise Training

Molecular and cellular biology, 2014-09, Vol.34 (18), p.3450-3460

2014

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PGC-1α Coactivates PDK4 Gene Expression via the Orphan Nuclear Receptor ERRα: a Mechanism for Transcriptional Control of Muscle Glucose Metabolism

Molecular and Cellular Biology, 2005-12, Vol.25 (24), p.10684-10694

2005

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Increased Glucose Availability Attenuates Myocardial Ketone Body Utilization

Journal of the American Heart Association, 2020-08, Vol.9 (15), p.e013039-e013039

2020

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Insulin receptor substrate signaling suppresses neonatal autophagy in the heart

The Journal of clinical investigation, 2013-12, Vol.123 (12), p.5319-5333

2013

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My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy

Diabetes and Metabolism Journal, 2017, 41(1), 159, pp.1-9

2017

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FGF21-FGFR4 signaling in cardiac myocytes promotes concentric cardiac hypertrophy in mouse models of diabetes

Scientific reports, 2022-05, Vol.12 (1), p.7326-7326, Article 7326

2022

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Diabetes-Related Cardiac Dysfunction

Endocrinology and Metabolism, 2017, 32(2), , pp.171-179

2017

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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

Molecular and cellular biology, 2015-03, Vol.35 (5), p.831-846

2015

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Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC‐1

The FASEB journal, 2002-12, Vol.16 (14), p.1879-1886

2002

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Insulin-Like Growth Factor I Receptor Signaling Is Required for Exercise-Induced Cardiac Hypertrophy

Molecular endocrinology (Baltimore, Md.), 2008-11, Vol.22 (11), p.2531-2543

2008

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Cardiac PI3K-Akt Impairs Insulin-Stimulated Glucose Uptake Independent of mTORC1 and GLUT4 Translocation

Molecular endocrinology (Baltimore, Md.), 2013-01, Vol.27 (1), p.172-184

2013

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Cardiomyocyte ZKSCAN3 regulates remodeling following pressure‐overload

Physiological reports, 2023-05, Vol.11 (9), p.e15686-n/a

2023

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PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis

PLoS biology, 2005-04, Vol.3 (4), p.e101-e101

2005

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Cardiac Energy Metabolism in Heart Failure

O-GlcNAcylation and cardiovascular disease

Metabolic Origins of Heart Failure

Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction

Role of O -Linked N -Acetylglucosamine Protein Modification in Cellular (Patho)Physiology

Editorial: Metabolic Regulation of Cardiac and Vascular Cell Function: Physiological and Pathophysiological Implications

Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice

Cardiomyocyte-Specific BMAL1 Plays Critical Roles in Metabolism, Signaling, and Maintenance of Contractile Function of the Heart

Redox biology and the interface between bioenergetics, autophagy and circadian control of metabolism

Mechanisms of Lipotoxicity in the Cardiovascular System

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

Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stress

Insulin Receptor Substrates Are Essential for the Bioenergetic and Hypertrophic Response of the Heart to Exercise Training

PGC-1α Coactivates PDK4 Gene Expression via the Orphan Nuclear Receptor ERRα: a Mechanism for Transcriptional Control of Muscle Glucose Metabolism

Increased Glucose Availability Attenuates Myocardial Ketone Body Utilization

Insulin receptor substrate signaling suppresses neonatal autophagy in the heart

My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy

FGF21-FGFR4 signaling in cardiac myocytes promotes concentric cardiac hypertrophy in mouse models of diabetes

Diabetes-Related Cardiac Dysfunction

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

Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC‐1

Insulin-Like Growth Factor I Receptor Signaling Is Required for Exercise-Induced Cardiac Hypertrophy

Cardiac PI3K-Akt Impairs Insulin-Stimulated Glucose Uptake Independent of mTORC1 and GLUT4 Translocation

Cardiomyocyte ZKSCAN3 regulates remodeling following pressure‐overload

PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis

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