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This meeting took place in 2013
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Meeting Details
Mitochondria, Metabolism and Myocardial Function — Basic Advances to Translational Studies (B1)
Organizer(s) Michael N. Sack and Roberta A. Gottlieb
February 3 - February 8, 2013
Keystone Resort • Keystone, Colorado USA
Abstract Deadline: October 3, 2012
Late Abstract Deadline: October 31, 2012
Scholarship Deadline: October 3, 2012
Early Registration Deadline: December 3, 2012
Supported by the Directors' Fund
CME Information
Summary of Meeting:
The most common causes of heart failure are coronary artery disease, high blood pressure and diabetes. Mitochondrial perturbations have been associated with heart failure itself and with most of the other preceding risk factors. In some cases mitochondrial dysfunction may play a causal role while in others mitochondria are a central target responsible for organ dysfunction. Understanding mitochondrial pathophysiology and identifying ways to ameliorate mitochondrial dysfunction are critical to therapy for cardiovascular disease. The continuous contractile function of the heart is required to sustain blood oxygenation, systemic circulation and nutrient supply to the body. This activity results in an unrelenting demand for energy production that is predominantly supported by mitochondrial oxidative phosphorylation. It is therefore not surprising that the mitochondria comprise about one third of cardiomyocyte volume, exhibit a promiscuous capacity to use energy substrates and possess biologic plasticity to maintain bioenergetic homeostasis. The centrality of mitochondria to sustain cardiac bioenergetics is additionally reflected in the development of cardiac pathology when mitochondria are dysfunctional. To counter this, a myriad of innate adaptive mitochondrial homeostatic programs are being identified. In the last two decades the investigations into mitochondrial biology with ever-increasing discovery technologies have enabled the scientific community to identify many novel programs controlling mitochondrial and metabolic function. The objectives of this conference are to: 1) Highlight the emerging adaptive programs identified in the heart orchestrating optimal mitochondrial homeostasis; 2) Review how the emerging risk factors of obesity and diabetes disrupt mitochondrial and cardiac function; and 3) Explore emerging metabolic targets for therapeutic interventions to modulate mitochondrial and metabolic perturbations associated with cardiac pathology.
CME Information
The most common causes of heart failure are coronary artery disease, high blood pressure and diabetes. Mitochondrial perturbations have been associated with heart failure itself and with most of the other preceding risk factors. In some cases mitochondrial dysfunction may play a causal role while in others mitochondria are a central target responsible for organ dysfunction. Understanding mitochondrial pathophysiology and identifying ways to ameliorate mitochondrial dysfunction are critical to therapy for cardiovascular disease. The continuous contractile function of the heart is required to sustain blood oxygenation, systemic circulation and nutrient supply to the body. This activity results in an unrelenting demand for energy production that is predominantly supported by mitochondrial oxidative phosphorylation. It is therefore not surprising that the mitochondria comprise about one third of cardiomyocyte volume, exhibit a promiscuous capacity to use energy substrates and possess biologic plasticity to maintain bioenergetic homeostasis. The centrality of mitochondria to sustain cardiac bioenergetics is additionally reflected in the development of cardiac pathology when mitochondria are dysfunctional. To counter this, a myriad of innate adaptive mitochondrial homeostatic programs are being identified. In the last two decades the investigations into mitochondrial biology with ever-increasing discovery technologies have enabled the scientific community to identify many novel programs controlling mitochondrial and metabolic function. The objectives of this conference are to: 1) Highlight the emerging adaptive programs identified in the heart orchestrating optimal mitochondrial homeostasis; 2) Review how the emerging risk factors of obesity and diabetes disrupt mitochondrial and cardiac function; and 3) Explore emerging metabolic targets for therapeutic interventions to modulate mitochondrial and metabolic perturbations associated with cardiac pathology.
Conference Program Print | View meeting in 12 hr (am/pm) time
SUNDAY, FEBRUARY 3
08:00—09:00
Welcome and Keynote Address
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*
Michael N. Sack,
NHLBI, National Institutes of Health, USA
*
Roberta A. Gottlieb,
San Diego State University, USA
Ana Maria Cuervo,
Albert Einstein College of Medicine, USA
Autophagy in the Cellular Energetic Balance
Autophagy in the Cellular Energetic Balance
09:00—12:00
The Biology of Mitochondrial Homeostatic Regulatory Programs and Cardiac Disease
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*
E. Dale Abel,
University of Utah School of Medicine, USA
*
Anne A. Knowlton,
University of California, Davis, USA
Roberta A. Gottlieb,
San Diego State University, USA
The Role of Mitophagy in Mitochondrial Biogenesis
The Role of Mitophagy in Mitochondrial Biogenesis
Gökhan S. Hotamisligil,
Harvard University, USA
Interactions between ER Stress and Mitochondrial Dysfunction in Metabolic Control
Interactions between ER Stress and Mitochondrial Dysfunction in Metabolic Control
Kinya Otsu,
King's College London, UK
Mitochondrial DNA in the Development of Cardiac Inflammation and Dysfunction
Mitochondrial DNA in the Development of Cardiac Inflammation and Dysfunction
Joseph A. Hill,
University of Texas Southwestern Medical Center, USA
Autophagy and the Failing Heart
Autophagy and the Failing Heart
Abhinav Diwan,
Washington University School of Medicine, USA
Short Talk: Transcription Factor EB Coordinates Mitochondrial Autophagy with Biogenesis
Short Talk: Transcription Factor EB Coordinates Mitochondrial Autophagy with Biogenesis
17:00—19:00
Regulation of Redox Stress in Cardiovascular Disease
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*
Lorrie A. Kirshenbaum,
University of Manitoba, St. Boniface Hospital Research Center, Canada
*
Satoaki Matoba†,
Kyoto Prefectural University of Medicine, Japan
Junichi Sadoshima,
University of Medicine and Dentistry of New Jersey, USA
Alternative Autophagy Mediates Mitochondrial Clearance in Response to Energy Stress
Alternative Autophagy Mediates Mitochondrial Clearance in Response to Energy Stress
John W. Elrod,
Temple School of Medicine, USA
Development of a Genome-Wide shRNA Screen to Identify Fundamental Pathways of Necrosis
Development of a Genome-Wide shRNA Screen to Identify Fundamental Pathways of Necrosis
Jan Dudek,
University of Goettingen, Germany
Short Talk: Respiratory Chain Remodeling in Barth Syndrome Patients
Short Talk: Respiratory Chain Remodeling in Barth Syndrome Patients
08:00—11:00
Metabolic Modulation in the Pathogenesis and Treatment of Cardiac Hypertrophy and Heart Failure
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*
Jason R. B. Dyck,
University of Alberta, Canada
*
P. Christian Schulze,
Columbia University, USA
Jan F. C. Glatz,
Maastricht University, Netherlands
Novel Signaling Pathways Regulating Substrate Switching in the Heart
Novel Signaling Pathways Regulating Substrate Switching in the Heart
Martin E. Young,
University of Alabama at Birmingham, USA
The Circadian Clock, Metabolic Regulation and Cardiac Pathology
The Circadian Clock, Metabolic Regulation and Cardiac Pathology
Gary D. Lopaschuk,
University of Alberta, Canada
Modulation of Malonyl-CoA and Cardiac Metabolic Consequences
Modulation of Malonyl-CoA and Cardiac Metabolic Consequences
William C. Stanley,
University of Sydney, Australia
Mitochondrial Pathology in Heart Failure: Novel Therapeutic Approaches
Mitochondrial Pathology in Heart Failure: Novel Therapeutic Approaches
Konstantinos Drosatos,
Columbia University, USA
Short Talk: PPARgamma Activation Prevents Cardiac Dysfunction in Sepsis via Stimulation of Energy Production and Prevention of Mitochondrial Loss
Short Talk: PPARgamma Activation Prevents Cardiac Dysfunction in Sepsis via Stimulation of Energy Production and Prevention of Mitochondrial Loss
17:00—19:00
Emerging Regulatory Programs in the Control of Mitochondria and Metabolism
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*
Robert S. Balaban,
NHLBI, National Institutes of Health, USA
*
Johan Auwerx,
École Polytechnique Fédérale de Lausanne (EPFL), Switzerland
Elizabeth Murphy,
NHLBI, National Institutes of Health, USA
S-Nitrosylation and Regulation of the Mitochondrial Stress Response
S-Nitrosylation and Regulation of the Mitochondrial Stress Response
Michael N. Sack,
NHLBI, National Institutes of Health, USA
Mitochondrial Protein Acetylation and the Control of Mitochondrial Metabolism
Mitochondrial Protein Acetylation and the Control of Mitochondrial Metabolism
Eric N. Olson,
University of Texas Southwestern Medical Center, USA
Control of Systemic Energy Homeostasis by Myogenic microRNAs and Mediator
Control of Systemic Energy Homeostasis by Myogenic microRNAs and Mediator
Christoph Koentges,
University of Freiburg, Germany
Short Talk: SIRT3 Deficiency Impairs Mitochondrial and Contractile Function But Not Post-Ischemic Contractile Recovery in the Heart
Short Talk: SIRT3 Deficiency Impairs Mitochondrial and Contractile Function But Not Post-Ischemic Contractile Recovery in the Heart
08:00—11:00
Nutrient Stressors and the Modulation of Cardiovascular Function
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*
Michael N. Sack,
NHLBI, National Institutes of Health, USA
*
Edward Miller,
Boston University, USA
Orian S. Shirihai,
Boston University, USA
The Interplay between Mitochondrial Bioenergetic Adaptation and Quality Control
The Interplay between Mitochondrial Bioenergetic Adaptation and Quality Control
E. Dale Abel,
University of Utah School of Medicine, USA
Obesity-Mediated Disruption of Cardiac Mitochondrial Function
Obesity-Mediated Disruption of Cardiac Mitochondrial Function
Jason R. B. Dyck,
University of Alberta, Canada
Caloric Restriction, Resveratrol and Cardiovascular Function
Caloric Restriction, Resveratrol and Cardiovascular Function
Daniel P. Kelly,
Sanford-Burnham Medical Research Institute, USA
Myocyte Lipotoxicity Screening to Delineate Mechanisms and Drug Targets
Myocyte Lipotoxicity Screening to Delineate Mechanisms and Drug Targets
P. Christian Schulze,
Columbia University, USA
Short Talk: Inhibition of de novo Ceramide Synthesis Improves Myocardial Function in Chronic Ischemic Cardiomyopathy
Short Talk: Inhibition of de novo Ceramide Synthesis Improves Myocardial Function in Chronic Ischemic Cardiomyopathy
17:00—19:00
Emerging Technologies to Characterize Mitochondrial and Metabolic Functioning
Meeting has ended...abstracts no longer viewable online. Purchase an Abstract Book from this meeting
*
Daniel P. Kelly,
Sanford-Burnham Medical Research Institute, USA
*
Elizabeth Murphy,
NHLBI, National Institutes of Health, USA
Robert S. Balaban,
NHLBI, National Institutes of Health, USA
Systems Biology of Cardiac Mitochondrion
Systems Biology of Cardiac Mitochondrion
Peipei Ping,
University of California, Los Angeles, USA
Metabolic Lessons from Unbiased Large-Scale Proteomics Studies in Mitochondria
Metabolic Lessons from Unbiased Large-Scale Proteomics Studies in Mitochondria
Christopher B. Newgard,
Duke University Medical Center, USA
Metabolomics Applied to Mitochondrial Dysfunction in Metabolic Diseases
Metabolomics Applied to Mitochondrial Dysfunction in Metabolic Diseases
Miguel A. Aon,
Johns Hopkins University, USA
Short Talk: Metabolomics Unveils the Adverse Metabolic Remodeling Elicited by Hyperglycemia and Mitochondrial Dysfunction, and its Relief by Palmitate in T2DM Heart
Short Talk: Metabolomics Unveils the Adverse Metabolic Remodeling Elicited by Hyperglycemia and Mitochondrial Dysfunction, and its Relief by Palmitate in T2DM Heart
08:00—11:00
Novel Programs Controlling Mitochondria and Metabolism
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*
Martin E. Young,
University of Alabama at Birmingham, USA
*
Peter A. Crawford,
Washington University School of Medicine, USA
Christine Des Rosiers,
Montreal Heart Institute (MHI), Canada
Metabolomics: What Have We Learned from Heart Failure Patients?
Metabolomics: What Have We Learned from Heart Failure Patients?
Johan Auwerx,
École Polytechnique Fédérale de Lausanne (EPFL), Switzerland
Protein Homeostasis in the Control of Mitochondrial Function and Aging
Protein Homeostasis in the Control of Mitochondrial Function and Aging
Thomas Langer,
University of Koeln, Germany
Mitochondrial Quality Control and Phospholipid Metabolism
Mitochondrial Quality Control and Phospholipid Metabolism
Catherine Le,
Colorado State University, USA
Short Talk: Integration of Respirometry and Metabo-Proteomic Profiling Reveal an Unexpected Mechanism of Cardiac Mitochondrial Dysfunction in Taz-Deficient Mice
Short Talk: Integration of Respirometry and Metabo-Proteomic Profiling Reveal an Unexpected Mechanism of Cardiac Mitochondrial Dysfunction in Taz-Deficient Mice
17:00—19:00
Clinical Studies to Advance Biological Insight and Therapeutic Targets
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*
Roberta A. Gottlieb,
San Diego State University, USA
*
Seigo Izumo†,
Takeda Pharmaceutical Company, Japan
Lawrence H. Young,
Yale University, USA
AMPK Regulates Mitochondrial Function during Myocardial Ischemia-Reperfusion
AMPK Regulates Mitochondrial Function during Myocardial Ischemia-Reperfusion
Patrick Schrauwen,
Maastricht University Medical Center, Netherlands
Lipotoxicity, Mitochondria and Cardiac Function: Insight from Human Clinical Intervention Studies
Lipotoxicity, Mitochondria and Cardiac Function: Insight from Human Clinical Intervention Studies
Anthony J. Muslin,
Novartis Institutes for BioMedical Research, USA
Akt2 Regulates Cardiac Structure and Function
Akt2 Regulates Cardiac Structure and Function
Yan Liu,
Massachusetts General Hospital, Harvard Medical School, USA
Short Talk: Small Molecules Selectively Alleviate Cardiotoxicity But Not Compromise Anti-Tumor Potency of Doxorubicin
Short Talk: Small Molecules Selectively Alleviate Cardiotoxicity But Not Compromise Anti-Tumor Potency of Doxorubicin
19:00—19:15
Closing Remarks
Meeting has ended...abstracts no longer viewable online. Purchase an Abstract Book from this meeting
Michael N. Sack,
NHLBI, National Institutes of Health, USA
Roberta A. Gottlieb,
San Diego State University, USA
*Session Chair †Speaker invited, not yet responded.
We gratefully acknowledge additional support for this conference from:
|
American Heart Association's Council on Basic Cardiovascular Sciences |
|
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