Mitochondria, Metabolism and Heart
joint with Angiogenesis and Vascular Disease
Organizer(s): Junichi Sadoshima, Toren Finkel and Åsa B. GustafssonDate: May 08 - 12, 2017
Location: Eldorado Hotel & Spa, Santa Fe, NM, USA
Mitochondria play a central role in regulating energy metabolism, redox status and cell death. The homeostasis of mitochondrial function is maintained by multiple mechanisms, collectively called mitochondrial quality control mechanisms. During the past decade, we have witnessed an explosion of research identifying novel mechanisms by which mitochondria control various cellular functions and cells maintain the homeostasis of mitochondria and metabolism in various cell types. Mitochondria are particularly abundant in the heart, and mitochondrial dysfunction and changes in cellular metabolism are commonly observed in failing or stressed hearts. However, there is a significant gap in our understanding of these mechanisms in cardiomyocytes and those in other cell types. The overall learning objectives of this meeting are to: 1) Understand how the novel functions of mitochondria contribute to the development or the prevention of myocardial injury and heart failure, and 2) Discuss how the quality of mitochondria is maintained in adult cardiomyocytes, whose mitochondrial dynamics are quite distinct from other commonly investigated cell types. Special emphasis will be placed on discussing the function and the mechanism of mitophagy; a novel mechanism of cell death mediated through autophagy; interaction between mitochondria dynamics and mitophagy; mitochondrial unfolded protein response (UPR) controlling aging, stress resistance and longevity; the role of metabolic intermediates as signaling mechanisms; and novel biomarkers identified through metabolomics analyses. With a joint session on angiogenesis shared with the meeting on “Angiogenesis and Vascular Disease,” attendees will get a quick overview regarding how mitochondria and metabolism regulate angiogenesis, a critical determinant for physiological versus pathological hypertrophy and ischemic injury. Overall, the audience will obtain better understanding regarding how the function of mitochondria is regulated in the heart, how it affects the overall function of the cardiovascular system, and how one intervenes with mitochondria and metabolism to achieve better treatment for heart failure and other cardiovascular diseases.
Scholarship Deadline: January 11 2017
Discounted Abstract Deadline: January 11 2017
Abstract Deadline: February 8 2017
Discounted Registration Deadline: March 8 2017
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:
We gratefully acknowledge the generous grant for this conference provided by:National Heart, Lung, and Blood Institute (NHLBI)
Grant No. 1R13HL137293-01
Funding for this conference was made possible (in part) by HL137293-01 from the National Heart, Lung and Blood Institute. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the NIH; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.