SFB 834: Endothelial Signalling and Vascular Repair

内皮活化或“功能障碍”通常被认为是心血管疾病发展期间血管内发生的最早可测量的变化之一，并且在减弱的内皮功能与不良患者预后之间存在有据可查的关系。已经详细研究了导致内皮功能障碍发展的机制，但是维持血管系统处于健康状态的保护性分子机制在很大程度上仍然难以捉摸。此外，还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形成。我们的合作研究中心（以下简称SFB 834）旨在确定在一系列基础科学，转化和临床项目中决定内皮细胞功能和修复的分子机制和细胞介质。总体长期目标是开发新的治疗概念并将其转移到临床。组成SFB 834的项目分为两大类：A部分的项目：“内皮信号转导”，主要侧重于维持内皮功能所必需的特定信号分子和分子机制。B部分“内皮细胞功能和修复”的项目是转化研究项目，旨在阐明风险因素（特别是与细胞代谢改变相关的风险因素）和内皮功能之间的相互作用，并通过细胞疗法改善心血管疾病的治疗。有几个项目侧重于分子的详细分析和已建立的信号通路，如一氧化氮，活性氧，G蛋白偶联受体等，以获得新的见解，他们的调节和参与心血管疾病。然而，SFB 834具有识别新兴优先领域并研究其在基础科学和转化研究水平上对血管研究的适用性的历史。因此，一个子项目集中在表观遗传调控的新机制，包括组蛋白修饰，microRNA，长非编码RNA和RNA剪接的调节剂。我们相信，这些新的新兴课题的阐明将提供至关重要的见解，心血管疾病的表观遗传控制，这可能会导致新的治疗靶点的发现。这是对血管壁的生理学和病理生理学和内皮细胞信号传导，血管修复和转化研究的特点SFB 834的整合的重点。

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.