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Web Desc
Mitochondria, Metabolism and Myocardial Function - Basic Advances to Translational Studies
Organizer(s): Michael N. Sack and Roberta A. Gottlieb
Date: February 03 - 08, 2013
Location: Keystone Resort, Keystone, CO, USA
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.
Scholarship Deadline: October 3 2012
Discounted Abstract Deadline: October 3 2012
Abstract Deadline: October 31 2012
Discounted Registration Deadline: December 3 2012
We gratefully acknowledge additional support for this conference from:
American Heart AssociationSeahorse Bioscience, Inc.


Zhiyong Cheng
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