pH 感知受体在结肠炎中的作用。

IF 2.9 4区 医学 Q2 PHYSIOLOGY Pflugers Archiv : European journal of physiology Pub Date : 2024-04-01 Epub Date: 2024-03-22 DOI:10.1007/s00424-024-02943-y
Martin Hausmann, Klaus Seuwen, Cheryl de Vallière, Moana Busch, Pedro A Ruiz, Gerhard Rogler
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引用次数: 0

摘要

肠道 pH 值过低与严重的炎症、纤维化和结直肠癌(CRC)有关,也是活动性炎症性肠病(IBD)的标志。因此,pH 感知机制对了解 IBD 病理生理学很有意义。组织缺氧和酸中毒是导致疾病病理生理学的两个因素,它们都与 IBD 有关,了解它们之间的相互作用与开发新的治疗方案密切相关。在一项大型全基因组关联研究中,质子感应 G 蛋白偶联受体(GPCR)家族的一个成员 GPR65(T 细胞死亡相关基因 8,TDAG8)被确定为 IBD 的易感基因。针对酸性细胞外 pH 值,GPR65 可诱导抗炎反应,而另外两种质子感应受体 GPR4 和 GPR68(卵巢癌 G 蛋白偶联受体 1,OGR1)则介导促炎反应。在此,我们回顾了目前关于这些质子感应受体在 IBD、IBD 相关纤维化和癌症以及结肠炎相关癌症(CAC)中的作用的知识。我们还介绍了这些受体的新兴小分子调节剂作为治疗 IBD 的治疗机会。
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Role of pH-sensing receptors in colitis.

Low pH in the gut is associated with severe inflammation, fibrosis, and colorectal cancer (CRC) and is a hallmark of active inflammatory bowel disease (IBD). Subsequently, pH-sensing mechanisms are of interest for the understanding of IBD pathophysiology. Tissue hypoxia and acidosis-two contributing factors to disease pathophysiology-are linked to IBD, and understanding their interplay is highly relevant for the development of new therapeutic options. One member of the proton-sensing G protein-coupled receptor (GPCR) family, GPR65 (T-cell death-associated gene 8, TDAG8), was identified as a susceptibility gene for IBD in a large genome-wide association study. In response to acidic extracellular pH, GPR65 induces an anti-inflammatory response, whereas the two other proton-sensing receptors, GPR4 and GPR68 (ovarian cancer G protein-coupled receptor 1, OGR1), mediate pro-inflammatory responses. Here, we review the current knowledge on the role of these proton-sensing receptors in IBD and IBD-associated fibrosis and cancer, as well as colitis-associated cancer (CAC). We also describe emerging small molecule modulators of these receptors as therapeutic opportunities for the treatment of IBD.

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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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