動脈硬化の分子機構

动脉硬化的分子机制

基本信息

批准号：
09281104
负责人：
KITA Toru
金额：
$ 165.89万
依托单位：
KYOTO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research on Priority Areas (A)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 2001
项目状态：
已结题

项目摘要

The Grants-in-Aid for Scientific Research on Priority Areas No. 09281104 was issued from 1997 to 2000. During the period, we organized a research group with scientists who are considered to be most active in the research field. Atherosclerosis is correlated with a variety of vascular disorders such as coronary heart disease. We therefore placed our goal on elucidation of the molecular mechanism of atherosclerosis and exploration of novel therapeutic strategies. To conduct investigation, the members were divided into 3 subgroups, i.e. Group 1, 2, and 3 with different subject of study as follows. We also formed a Central Committee to coordinate and facilitate the research activity of the subgroups.[Group 1] Study subject : Molecular mechanism of vascular formation. Atherosclerosis has been considered to evolve according to the mechanism shared with vascular formation in the body. During the research period, we have made a significant progress in understanding vasculogenesis and angiogene … More sis. In Conclusion, the roles of new molecules such as transcription factor ets-1 and other molecules were clarified. [Group 2] Study subject : Endothelial dysfunction and blood cells. There has been accumulating evidence that atherosclerosis is initiated by endothelial dysfunction due to a variety of biological insults. We therefore formed this subgroup to explore the key molecules involved in those events. We discovered novel scavenger receptors such as LOX-1 and SRPSOX. Furthermore, we revealed that adipose tissues produce cytokines abundantly. Among those cytokines, adiponectin has been shown to play an important role in atherogenesis and insulin resistance. [Group 3] Study subject : Molecular mechanism of phenotypical conversion and proliferation of vascular smooth muscle cells. This subgroup focused on the mechanism of phenotypical conversion of vascular smooth muscle cells, which is believed to be the characteristic feature of the advanced atherosclerotic lesions. To clarify these points, a variety of transcription factors such as BTBE2 were examined. Also, the new methods to deliver genes were developed.In conclusion, we have made a successful progress in atherosclerosis research, which will be translated into clinical application in the near future. Less

1997年至2000年发放了第09281104号优先领域科学研究补助金。在此期间，我们组织了一个由动脉粥样硬化与动脉粥样硬化研究领域最活跃的科学家组成的研究小组。因此，我们的目标是阐明动脉粥样硬化的分子机制并探索新的治疗策略。成员分为三个小组，即小组1、小组2和小组3，其研究主题如下。我们还成立了一个中央委员会来协调和促进小组的研究活动。 [小组1] 研究主题：分子机制。动脉粥样硬化被认为是按照与体内血管形成相同的机制进化的。在研究期间，我们在了解血管生成和血管生成方面取得了重大进展……更多总之，转录因子 ets-1 和其他分子的作用已得到阐明。 [组 2] 研究主题：内皮功能障碍和血细胞越来越多的证据表明，动脉粥样硬化是由内皮功能障碍引起的。因此，我们成立了这个小组来探索参与这些事件的关键分子，例如 LOX-1 和 SRPSOX。脂肪组织产生大量细胞因子，其中脂联素已被证明在动脉粥样硬化形成和胰岛素抵抗中发挥重要作用。 [组3] 研究主题：血管平滑肌细胞表型转化和增殖的分子机制。血管平滑肌细胞表型转换的机制被认为是晚期动脉粥样硬化病变的特征。为了阐明这些观点，研究了多种转录因子，例如 BTBE2。总而言之，我们在动脉粥样硬化研究方面取得了成功，并将在不久的将来转化为临床应用。