Sands William A, Palmer Timothy M
Molecular Pharmacology Group, Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, Scotland, UK.
Immunol Lett. 2005 Oct 15;101(1):1-11. doi: 10.1016/j.imlet.2005.04.005. Epub 2005 Apr 26.
The nucleoside adenosine accumulates in many tissues following the onset of ischaemia and inflammation. This initiates a series of protective mechanisms in target cells upon binding and activation of a family of four G-protein-coupled cell surface adenosine receptor (AR) proteins. The magnitude and duration of adenosine's effects are dictated by the identity and expression levels of each receptor subtype on individual cell types within the hypoxic microenvironment. Given the key role of endothelial cells (ECs) in the development of inflammatory diseases, such as sepsis, rheumatoid arthritis (RA) and atherosclerosis, ARs represent attractive targets for therapeutic intervention in these conditions. In this review, we examine several critical aspects of endothelial function in vivo, assess the role of individual AR subtypes in these events and, where known, discuss the molecular mechanisms by which specific ARs exert their effects.
缺血和炎症发生后，核苷腺苷会在许多组织中蓄积。腺苷与四种G蛋白偶联细胞表面腺苷受体（AR）蛋白家族结合并激活后，会在靶细胞中启动一系列保护机制。在缺氧微环境中，腺苷作用的强度和持续时间取决于各受体亚型在不同细胞类型上的特性和表达水平。鉴于内皮细胞（ECs）在脓毒症、类风湿性关节炎（RA）和动脉粥样硬化等炎症性疾病发展过程中的关键作用，腺苷受体是这些疾病治疗干预的有吸引力的靶点。在本综述中，我们研究了体内内皮功能的几个关键方面，评估了各AR亚型在这些事件中的作用，并在已知的情况下讨论了特定AR发挥作用的分子机制。
