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G 蛋白偶联受体在急性肾损伤中的作用。

Role of G protein coupled receptors in acute kidney injury.

机构信息

Department of Nephrology, the Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University, Third Military Medical University), Chongqing, 400037, China.

出版信息

Cell Commun Signal. 2024 Sep 2;22(1):423. doi: 10.1186/s12964-024-01802-8.

DOI:10.1186/s12964-024-01802-8
PMID:39223553
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11367933/
Abstract

Acute kidney injury (AKI) is a clinical condition characterized by a rapid decline in kidney function, which is associated with local inflammation and programmed cell death in the kidney. The G protein-coupled receptors (GPCRs) represent the largest family of signaling transduction proteins in the body, and approximately 40% of drugs on the market target GPCRs. The expressions of various GPCRs, prostaglandin receptors and purinergic receptors, to name a few, are significantly altered in AKI models. And the role of GPCRs in AKI is catching the eyes of researchers due to their distinctive biological functions, such as regulation of hemodynamics, metabolic reprogramming, and inflammation. Therefore, in this review, we aim to discuss the role of GPCRs in the pathogenesis of AKI and summarize the relevant clinical trials involving GPCRs to assess the potential of GPCRs and their ligands as therapeutic targets in AKI and the transition to AKI-CKD.

摘要

急性肾损伤 (AKI) 是一种以肾功能迅速下降为特征的临床病症,与肾脏局部炎症和程序性细胞死亡有关。G 蛋白偶联受体 (GPCR) 是体内最大的信号转导蛋白家族,约有 40%的上市药物以 GPCR 为靶点。在 AKI 模型中,各种 GPCR、前列腺素受体和嘌呤能受体等的表达均发生显著改变。由于 GPCR 具有调节血液动力学、代谢重编程和炎症等独特的生物学功能,因此其在 AKI 中的作用引起了研究人员的关注。因此,在本综述中,我们旨在讨论 GPCR 在 AKI 发病机制中的作用,并总结涉及 GPCR 的相关临床试验,以评估 GPCR 及其配体作为 AKI 和 AKI-CKD 转化治疗靶点的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/4d9119f609ee/12964_2024_1802_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/48e80ec9295c/12964_2024_1802_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/f79e63fb8f91/12964_2024_1802_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/4d9119f609ee/12964_2024_1802_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/48e80ec9295c/12964_2024_1802_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/f79e63fb8f91/12964_2024_1802_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f1b/11367933/4d9119f609ee/12964_2024_1802_Fig3_HTML.jpg

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