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

慢性和间歇性低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危险因素。 失败了。慢性缺氧性肺病，如慢性阻塞性肺疾病，会导致肺动脉高压和右心衰竭。 然而，氧分压变化可能影响心力衰竭发病机制的机制， 还没有被定义。这种知识的缺乏干扰了新的预防战略的制定 和/或治疗与缺氧性疾病相关的心力衰竭。我们的长远目标是促进一体化和 建立缺氧性心力衰竭机制的跨学科研究。这样做的目的是 应用程序是将来自不同学科的领先研究人员聚集在一起，就 氧感应机制与心力衰竭发生发展的关系。该计划的基本原理 拟议的研讨会是，一旦了解氧气感应和心力衰竭之间的关系 机制已经获得，这将导致可用于预防和/或治疗心脏的新策略 与肺部疾病和睡眠呼吸暂停相关的衰竭。应用程序的目标将会实现 通过回答四个具体问题：1)氧气感应的机制是什么？2)氧气感应的 心肌肥大和衰竭的机制？3)氧感应/缺氧如何影响发病机制 心肌肥厚和衰竭？4)氧化还原信号在相互作用机制中起什么作用 氧感应/缺氧与心肌肥厚/衰竭之间的关系？在为期两天半的研讨会期间 会议将于2006年10月11日至13日在华盛顿特区举行。拟议的研讨会具有创新性 因为它将汇集来自不同学科的研究人员，包括涉及呼吸系统的研究人员， 神经学和心血管研究，并将为年轻研究人员提供参与 讨论。我们期望拟议的讲习班将促进综合性和跨学科 关于低氧对心肌肥厚/衰竭影响的研究尚不多见的领域包括 右心衰竭的机制。这些结果将是重要的，因为他们预计将提供 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，结果显示， 将从根本上推动肺生物学和心脏生物学领域的发展。

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.