Molecular Biology of Cardiac Diseases and Regeneration
Organizer(s): Elizabeth McNally and Jonathan A. EpsteinDate: April 03 - 08, 2005
Location: Sheraton Steamboat Resort, Steamboat Springs, CO, USA
Cardiovascular disease is the leading cause of morbidity and mortality in the United States. Myocardial infarction and congestive heart failure, together, account for the majority of cardiovascular disease. An underlying theme in both myocardial infarction and congestive heart failure is an insufficient number of properly functioning cardiomyocytes. Repairing defective cardiomyocytes and/or regenerating cardiomyocytes are important experimental means to improve heart function. To this end, stem cells from embryonic and adult sources have been increasingly explored as a means of restoring cardiac function. Vascular growth remains a significant concern since vascular supply is essential to the survival of regenerated cardiomyocytes. To establish a fully functioning cardiomyocyte requires a detailed understanding of cardiomyocyte differentiation as well as a pluripotent stem cell capable of achieving the cardiomyocyte developmental pathway. At the cellular level, cardiomyocyte dysfunction arises from ischemic insult, genetic or toxic metabolic defects. The broad etiology responsible for the dysfunctioning cardiomyocyte has not limited the identification of molecular pathways in common to these many different forms of heart failure. Defects of intracellular calcium homeostasis are a frequent issue in failing cardiomyocytes. Perturbations of calcium homeostasis directly affect sarcomere function and simultaneously render an altered signaling cascade. The goal of this meeting is twofold. We will discuss cellular and molecular pathways necessary for cardiac regeneration. This will include a discussion of stem cell choice as well as a full evaluation of current stem cell transplant programs with an emphasis on full integration and differentiation of the transplanted stem cell. The second major emphasis of the meeting will be to discuss the failing cardiomyocyte focused on the common and critical molecular pathways found in the diseased cardiomyocyte. These two broad areas overlap considerably since both approaches will be required to successfully repair a failed cardiomyocyte.
Discounted Abstract Deadline: December 2 2004
Discounted Registration Deadline: February 3 2005
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:
Osiris Therapeutics, Inc.