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This meeting took place in 2013
Here are the related meetings in 2021:
Mitochondria, Metabolism and Heart - RESCHEDULING IN PROGRESS (J1)
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Mitochondria, Metabolism and Myocardial Function - Basic Advances to Translational Studies (B1)
Organizer(s) Michael N. Sack and Roberta A. Gottlieb
February 3—8, 2013
Keystone Resort • Keystone, CO USA
Abstract Deadline: Oct 3, 2012
Late Abstract Deadline: Oct 31, 2012
Scholarship Deadline: Oct 3, 2012
Early Registration Deadline: Dec 3, 2012
Supported by the Directors' Fund
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.
View Scholarships/Awards
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.
View Scholarships/Awards
No registration fees are used to fund entertainment or alcohol at this conference
SUNDAY, FEBRUARY 3
MONDAY, FEBRUARY 4
TUESDAY, FEBRUARY 5
WEDNESDAY, FEBRUARY 6
THURSDAY, FEBRUARY 7
FRIDAY, FEBRUARY 8
Conference Program Print | View meeting in 12 hr (am/pm) time
SUNDAY, FEBRUARY 3
08:00—09:00
Welcome and Keynote Address
*
Michael N. Sack,
NHLBI, National Institutes of Health, USA
*
Roberta A. Gottlieb,
Cedars-Sinai Medical Center, USA
Ana Maria Cuervo,
Albert Einstein College of Medicine, USA
Selective Autophagy and the Cellular Energetic Balance
Selective Autophagy and the Cellular Energetic Balance
09:00—12:00
The Biology of Mitochondrial Homeostatic Regulatory Programs and Cardiac Disease
*
E. Dale Abel,
University of Iowa, Carver College of Medicine, USA
*
Anne A. Knowlton,
University of California, Davis, USA
Gökhan S. Hotamisligil,
Harvard School of Public Health, USA
Interactions between ER Stress and Mitochondrial Dysfunction in Metabolic Control
Interactions between ER Stress and Mitochondrial Dysfunction in Metabolic Control
Kinya Otsu,
, 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 in Cardiac Plasticity
Autophagy in Cardiac Plasticity
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
*
Lorrie A. Kirshenbaum,
University of Manitoba, Canada
*
Satoaki Matoba†,
Kyoto Prefectural University of Medicine, Japan
Junichi Sadoshima,
Rutgers New Jersey Medical School, USA
Alternative Autophagy Mediates Mitochondrial Clearance in Response to Energy Stress
Alternative Autophagy Mediates Mitochondrial Clearance in Response to Energy Stress
Gerald S. Shadel,
The Salk Institute for Biological Studies, USA
Mitochondrial Stress Signaling in Disease and Aging
Mitochondrial Stress Signaling in Disease and Aging
John W. Elrod,
Lewis Katz School of Medicine at Temple University, USA
Building a Roadmap of Necrotic Cell Death
Building a Roadmap of Necrotic Cell Death
Jan Dudek,
University of Goettingen, Germany
Short Talk: Cardiolipin Deficiency Affects Respiratory Chain Organization and Function
Short Talk: Cardiolipin Deficiency Affects Respiratory Chain Organization and Function
08:00—11:00
Metabolic Modulation in the Pathogenesis and Treatment of Cardiac Hypertrophy and Heart Failure
*
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,
Temple University School of Medicine, 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
*
Robert S. Balaban,
NHLBI, National Institutes of Health, USA
*
Johan Auwerx,
École Polytechnique Fédérale de Lausanne, 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
Acetylation in the Control of Mitochondrial Homeostasis and Mitophagy
Acetylation in the Control of Mitochondrial Homeostasis and Mitophagy
Eric N. Olson,
University of Texas Southwestern Medical Center, USA
A Myocardial Metabolic Axis Controlled by Med13
A Myocardial Metabolic Axis Controlled by Med13
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
*
Michael N. Sack,
NHLBI, National Institutes of Health, USA
*
Edward Miller,
Boston University, USA
Orian S. Shirihai,
University of California, Los Angeles, USA
Mitochondrial Dynamics in Quality Control and Bioenergetics
Mitochondrial Dynamics in Quality Control and Bioenergetics
E. Dale Abel,
University of Iowa, Carver College of Medicine, USA
Obesity and Fatty Acid-Mediated Disruption of Cardiac Mitochondrial Function and Autophagy
Obesity and Fatty Acid-Mediated Disruption of Cardiac Mitochondrial Function and Autophagy
Jason R. B. Dyck,
University of Alberta, Canada
Caloric Restriction, Resveratrol and Cardiovascular Function
Caloric Restriction, Resveratrol and Cardiovascular Function
Daniel P. Kelly,
University of Pennsylvania, 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
*
Daniel P. Kelly,
University of Pennsylvania, USA
*
Elizabeth Murphy,
NHLBI, National Institutes of Health, USA
Robert S. Balaban,
NHLBI, National Institutes of Health, USA
Systems Biology of the Mitochondria Coordinated Moldulation of Complex Activity
Systems Biology of the Mitochondria Coordinated Moldulation of Complex Activity
Peipei Ping,
University of California, Los Angeles, USA
Large-Scale Proteomics Characterization of Cardiac Mitochondria: Molecular Function and Dynamics
Large-Scale Proteomics Characterization of Cardiac Mitochondria: Molecular Function and Dynamics
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
*
Martin E. Young,
University of Alabama at Birmingham, USA
*
Peter A. Crawford,
University of Minnesota, 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, Switzerland
Mitochondrial Function and Aging
Mitochondrial Function and Aging
Thomas Langer,
CECAD Research Center, 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
*
Roberta A. Gottlieb,
Cedars-Sinai Medical Center, 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, 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,
Tectonic Therapeutic, Inc., USA
Akt2 Regulates Cardiac Structure and Function
Akt2 Regulates Cardiac Structure and Function
Yan Liu,
Massachusetts General Hospital, Harvard Medical School, USA
Short Talk: Discovering Cardioprotective Drugs with Zebrafish
Short Talk: Discovering Cardioprotective Drugs with Zebrafish
19:00—19:15
Closing Remarks
Michael N. Sack,
NHLBI, National Institutes of Health, USA
Roberta A. Gottlieb,
Cedars-Sinai Medical Center, USA
*Session Chair †Invited, not yet responded.
We gratefully acknowledge support for this conference from:
We gratefully acknowledge additional support for this conference from:
|
American Heart Association's Council on Basic Cardiovascular Sciences |
|
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