School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.
School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales, Australia.
Br J Pharmacol. 2024 Jul;181(14):2197-2211. doi: 10.1111/bph.16059. Epub 2023 Mar 2.
Inflammatory bowel disease (IBD) is a chronic debilitating condition, hallmarked by persistent inflammation of the gastrointestinal tract. Despite recent advances in clinical treatments, the aetiology of IBD is unknown, and a large proportion of patients are refractory to pharmacotherapy. Understanding IBD immunopathogenesis is crucial to discern the cause of IBD and optimise treatments. Mas-related G protein-coupled receptors (Mrgprs) are a family of approximately 50 G protein-coupled receptors that were first identified over 20 years ago. Originally known for their expression in skin nociceptors and their role in transmitting the sensation of itch in the periphery, new reports have described the presence of Mrgprs in the gastrointestinal tract. In this review, we consider the impact of these findings and assess the evidence that suggests that Mrgprs may be involved in the disrupted homeostatic processes that contribute to gastrointestinal disorders and IBD. LINKED ARTICLES: This article is part of a themed issue Therapeutic Targeting of G Protein-Coupled Receptors: hot topics from the Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists 2021 Virtual Annual Scientific Meeting. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.14/issuetoc.
炎症性肠病(IBD)是一种慢性衰弱性疾病,其特征为胃肠道持续炎症。尽管临床治疗最近取得了进展,但 IBD 的病因尚不清楚,很大一部分患者对药物治疗有抗药性。了解 IBD 的免疫发病机制对于辨别 IBD 的病因和优化治疗至关重要。Mas 相关 G 蛋白偶联受体(Mrgprs)是一个大约 50 个 G 蛋白偶联受体的家族,它们在 20 多年前首次被发现。最初因其在皮肤伤害感受器中的表达及其在外周传递瘙痒感的作用而闻名,新的报道描述了 Mrgprs 存在于胃肠道中。在这篇综述中,我们考虑了这些发现的影响,并评估了表明 Mrgprs 可能参与导致胃肠道疾病和 IBD 的破坏内稳态过程的证据。相关文章:本文是治疗性靶向 G 蛋白偶联受体特刊的一部分:2021 年澳大利亚临床和实验药理学和毒理学学会虚拟年会的热门话题。要查看本节中的其他文章,请访问 http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.14/issuetoc.