Integrative Cardio-Pulmonary Workshop: From Oxygen Sensing to Heart Failure

慢性和间歇性缺氧对各种肺部疾病和睡眠障碍的反应已被证明， 与心力衰竭有关。例如，阻塞性睡眠呼吸暂停是高血压和心脏病的风险 失败慢性低氧性肺病如COPD会导致肺动脉高压和右心衰竭。 然而，氧张力变化如何影响心力衰竭发病机制的机制， 尚未定义。缺乏这方面的知识会妨碍制定新的战略， 和/或治疗与缺氧性疾病相关的心力衰竭。我们的长期目标是促进一体化， 跨学科的研究，以建立缺氧引起的心力衰竭的机制。的目的 应用程序是汇集来自不同学科的领先研究人员进行互动和讨论， 氧传感机制与心力衰竭发展之间的关系。的理由 提出的研讨会是，一旦了解氧传感和心力衰竭之间的关系， 机制已经获得，它将导致新的策略，可用于预防和/或治疗心脏病 与肺部疾病和睡眠呼吸暂停相关的衰竭。申请的目的将得以实现 通过解决四个具体问题：1）氧传感的机制是什么？2)有哪些 心脏肥大和衰竭的机制3)氧感/缺氧如何影响发病机制 心脏肥大和衰竭4)氧化还原信号在相互作用机制中的作用是什么 氧感/缺氧和心脏肥大/衰竭之间的关系？在为期两天半的研讨会上， 将于2006年10月11日至13日在华盛顿举行。拟议的讲习班具有创新性 因为它将汇集来自不同学科的研究人员，包括呼吸系统， 神经和心血管研究，并将为年轻的研究人员提供参与的机会， 讨论。我们期望拟议的讲习班将促进综合和跨学科的 关于缺氧对心脏肥大/衰竭影响的尚未充分研究的领域的研究，包括 右心衰竭的机制这些结果将是重要的，因为它们预计将提供 治疗睡眠呼吸暂停和肺动脉高压相关心力衰竭的新药物。此外，结果 将从根本上推进肺和心脏生物学领域。

Chronic and intermittent hypoxia in response to various lung diseases and sleep disorders has been shown to be associated with heart failure. For example, obstructive sleep apnea is a risk for hypertension and heart failure. Chronic hypoxic lung diseases such as COPD result in pulmonary hypertension and right heart failure. Mechanisms of how changes in oxygen tension might influence the pathogenesis of heart failure, however, have not been defined. Lack of such knowledge interferes with the development of new strategies to prevent and/or treat heart failure associated with hypoxic disorders. Our long-range goal is to promote integrative and interdisciplinary research to establish mechanisms of hypoxia-induced heart failure. The objective of this application is to bring together leading investigators from various disciplines to interact and discuss about the relationships between oxygen sensing mechanisms and the development of heart failure. The rationale for the proposed Workshop is that, once knowledge of the relationship between oxygen sensing and heart failure mechanisms has been obtained, it will lead to new strategies that can be used to prevent and/or treat heart failure associated with lung diseases and sleep apnea. The objective of the application will be accomplished by addressing four specific questions: 1) What are the mechanisms of oxygen sensing? 2) What are the mechanisms of cardiac hypertrophy and failure? 3) How does oxygen sensing/hypoxia affect the pathogenesis of cardiac hypertrophy and failure? 4) What are the roles of redox signaling in the mechanism of interactions between oxygen sensing/hypoxia and cardiac hypertrophy/failure? during the two and a half-day Workshop which will be held from Oct. 11th to 13th, 2006 in Washington DC. The proposed Workshop is innovative because it will bring together investigators from various disciplines including those involved in respiratory, neurological and cardiovascular research and will provide opportunities for young investigators to participate in discussions. It is our expectation that the proposed Workshop will stimulate integrative and interdisciplinary research on yet under-studied areas concerning the effects of hypoxia on cardiac hypertrophy/failure including the mechanism of right heart failure. These results will be significant because they are expected to provide new agents against sleep apnea- and pulmonary hypertension-associated heart failure. In addition, the results will fundamentally advance the fields of pulmonary and cardiac biology.