SFB 834: Endothelial Signalling and Vascular Repair

SFB 834：内皮信号传导和血管修复

• 批准号: 75732319
• 金额: --
• 依托单位: Goethe-Universität Frankfurt am Main
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2010
• 资助国家: 德国
• 起止时间: 2009-12-31 至 2020-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/75732319?language=en
• 关键词: SFB; 834; Endothelial; Signalling; Vascular

Endothelial activation or “dysfunction” is generally accepted to be one of the earliest measurable changes to take place within vessels during cardiovascular disease development and there is a well-documented relationship between attenuated endothelial function and poor patient prognosis. The mechanisms that contribute to the development of endothelial dysfunction have been investigated in detail but the protective molecular mechanisms that maintain the vasculature in a healthy state remain largely elusive. Moreover, it is unclear how endogenous cellular repair mechanisms/processes can improve endothelial cell function and neovascularisation. Our Collaborative Research Centre (hereafter referred to as SFB 834) aims to identify the molecular mechanisms and cellular mediators that determine endothelial cell function and repair in a series of basic science, translational and clinical projects. The overall long-term goal is the development of new therapeutic concepts and their transfer to the clinic. The projects making up SFB 834 are grouped under two general headings: projects in part A: “Endothelial Signaltransduktion”, focus largely on specific signalling molecules and molecular mechanisms that are necessary for the maintenance of endothelial function. The projects in part B “Endothelial Cell Function and Repair” are translational research projects that aim to elucidate the interaction between risk factors (especially those associated with altered cellular metabolism) and endothelial function and to improve the treatment of cardiovascular disease by cell therapy. Several projects focus on the detailed analysis of molecules and established signalling pathways such as nitric oxide, reactive oxygen species, G-protein coupled receptors etc. to gain novel insight into their regulation and participation in cardiovascular disease. However, SFB 834 has a history of identifying emerging priority areas and studying their applicability to vascular research at the basic science and translational research levels. Thus, a subsection of projects focuses on novel mechanisms of epigenetic regulation including regulators of histone modification, microRNAs, long non coding RNAs and RNA splicing. We believe that the elucidation of these novel emerging topics will provide crucial insights into the epigenetic control of cardiovascular diseases, which may lead to the discovery of novel therapeutic targets. It is this focus on the physiology and pathophysiology of the vessel wall and the integration of endothelial cell signalling, vascular repair and translational research that characterises SFB 834.

内皮激活或“功能障碍”通常被认为是心血管疾病发育期间维斯氏症发生的最早的可测量变化之一，并且衰减的内皮功能与患者预后不良之间存在据可查的关系。已经详细研究了有助于内皮功能障碍发展的机制，但是在健康状态下保持脉管系统的保护分子机制仍然在很大程度上难以捉摸。此外，尚不清楚内源性细胞修复机制/过程如何改善内皮细胞功能和新血管造成。我们的合作研究中心（以下称为SFB 834）旨在确定在一系列基础科学，翻译和临床项目中确定内皮细胞功能和修复的分子机制和细胞介质。总体长期目标是发展新的治疗概念及其转移到诊所。构成SFB 834的项目分组在两个通用标题下：A部分：“内皮信号传输”，主要集中在特定信号分子和维持内皮功能所必需的分子机制上。 B部分“内皮细胞功能和修复”中的项目是翻译的研究项目，旨在阐明危险因素（尤其是与细胞代谢改变的危险因素）和内皮功能之间的相互作用，并通过细胞疗法改善了心血管疾病的治疗。几个项目着重于分子和已建立的信号通路的详细分析，例如一氧化氮，活性氧，G蛋白偶联受体等，以获得对其调节和参与心血管疾病的新见解。但是，SFB 834具有识别新兴优先领域并研究其对基础科学和转化研究水平血管研究的适用性的历史。这是项目的一部分侧重于表观遗传调节的新机制，包括组蛋白修饰的调节剂，microRNA，长期非编码RNA和RNA剪接。我们认为，阐明这些新型新兴主题将为心血管疾病的表观遗传控制提供至关重要的见解，这可能导致发现新型治疗靶标。正是这种侧重于血管壁的生理和病理生理学以及象征SFB 834的内皮细胞信号传导，血管修复和翻译研究的整合。