• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

采用GPR75治疗肥胖症：揭示这种孤儿GPCR的已知与未知情况。

Adopting GPR75 in treating obesity: unraveling the knowns and unknowns of this orphan GPCR.

作者信息

Jiang Yiao, Zhang Zhao

机构信息

Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Endocrinology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Division of Endocrinology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Trends Cell Biol. 2025 Feb;35(2):102-104. doi: 10.1016/j.tcb.2024.12.006. Epub 2025 Jan 9.

DOI:10.1016/j.tcb.2024.12.006
PMID:39794254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11805625/
Abstract

G protein-coupled receptor 75 (GPR75) is emerging as a promising target for obesity treatment, but its exact role in energy regulation remains unclear. This article explores the latest research on GPR75's molecular function, potential ligands, and therapeutic challenges in addressing obesity.

摘要

G蛋白偶联受体75（GPR75）正逐渐成为肥胖治疗的一个有前景的靶点，但其在能量调节中的具体作用仍不清楚。本文探讨了关于GPR75分子功能、潜在配体以及肥胖治疗挑战的最新研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/11805625/1ea7c5090190/nihms-2042326-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/11805625/1ea7c5090190/nihms-2042326-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c32/11805625/1ea7c5090190/nihms-2042326-f0001.jpg

相似文献

1
Adopting GPR75 in treating obesity: unraveling the knowns and unknowns of this orphan GPCR.采用GPR75治疗肥胖症：揭示这种孤儿GPCR的已知与未知情况。
Trends Cell Biol. 2025 Feb;35(2):102-104. doi: 10.1016/j.tcb.2024.12.006. Epub 2025 Jan 9.
2
G Protein-Coupled Receptor 75 (GPR75) As a Novel Molecule for Targeted Therapy of Cancer and Metabolic Syndrome.G 蛋白偶联受体 75（GPR75）作为癌症和代谢综合征靶向治疗的新分子。
Asian Pac J Cancer Prev. 2023 May 1;24(5):1817-1825. doi: 10.31557/APJCP.2023.24.5.1817.
3
Mice deficient for G-protein-coupled receptor 75 display altered presynaptic structural protein expression and disrupted fear conditioning recall.G 蛋白偶联受体 75 缺失的小鼠表现出突触前结构蛋白表达改变和恐惧条件反射记忆缺失。
J Neurochem. 2023 Jun;165(6):827-841. doi: 10.1111/jnc.15818. Epub 2023 Apr 21.
4
Ciliary localization of GPR75 promotes fat accumulation in mice.GPR75 的纤毛定位促进了小鼠脂肪的积累。
J Clin Invest. 2024 Oct 1;134(19):e185059. doi: 10.1172/JCI185059.
5
Central regulation of feeding and body weight by ciliary GPR75.通过纤毛 GPR75 对摄食和体重的中枢调节。
J Clin Invest. 2024 Aug 13;134(19):e182121. doi: 10.1172/JCI182121.
6
20-HETE Signals Through G-Protein-Coupled Receptor GPR75 (G) to Affect Vascular Function and Trigger Hypertension.20-羟基二十碳四烯酸（20-HETE）通过G蛋白偶联受体GPR75发出信号，影响血管功能并引发高血压。
Circ Res. 2017 May 26;120(11):1776-1788. doi: 10.1161/CIRCRESAHA.116.310525. Epub 2017 Mar 21.
7
An orphan to the rescue of obesity and steatotic liver?孤儿能拯救肥胖和脂肪肝吗？
Trends Endocrinol Metab. 2024 Sep;35(9):761-762. doi: 10.1016/j.tem.2024.06.012. Epub 2024 Jun 29.
8
Loss of GPR75 protects against non-alcoholic fatty liver disease and body fat accumulation.GPR75 缺失可预防非酒精性脂肪性肝病和体脂肪堆积。
Cell Metab. 2024 May 7;36(5):1076-1087.e4. doi: 10.1016/j.cmet.2024.03.016. Epub 2024 Apr 22.
9
The orphan G-protein-coupled receptor 75 signaling is activated by the chemokine CCL5.孤儿 G 蛋白偶联受体 75 的信号由趋化因子 CCL5 激活。
J Neurochem. 2018 Sep;146(5):526-539. doi: 10.1111/jnc.14463. Epub 2018 Aug 2.
10
Global and endothelial G-protein coupled receptor 75 (GPR75) knockout relaxes pulmonary artery and mitigates hypoxia-induced pulmonary hypertension.全球和内皮 G 蛋白偶联受体 75（GPR75）敲除可使肺动脉松弛并减轻缺氧诱导的肺动脉高压。
Vascul Pharmacol. 2023 Dec;153:107235. doi: 10.1016/j.vph.2023.107235. Epub 2023 Sep 23.

本文引用的文献

1
Ciliary localization of GPR75 promotes fat accumulation in mice.GPR75 的纤毛定位促进了小鼠脂肪的积累。
J Clin Invest. 2024 Oct 1;134(19):e185059. doi: 10.1172/JCI185059.
2
Central regulation of feeding and body weight by ciliary GPR75.通过纤毛 GPR75 对摄食和体重的中枢调节。
J Clin Invest. 2024 Aug 13;134(19):e182121. doi: 10.1172/JCI182121.
3
Loss of GPR75 protects against non-alcoholic fatty liver disease and body fat accumulation.GPR75 缺失可预防非酒精性脂肪性肝病和体脂肪堆积。
Cell Metab. 2024 May 7;36(5):1076-1087.e4. doi: 10.1016/j.cmet.2024.03.016. Epub 2024 Apr 22.
4
Gpr75 knockout mice display age-dependent cone photoreceptor cell loss.Gpr75 敲除小鼠表现出与年龄相关的视锥细胞丢失。
J Neurochem. 2023 Nov;167(4):538-555. doi: 10.1111/jnc.15979. Epub 2023 Oct 15.
5
Mice deficient for G-protein-coupled receptor 75 display altered presynaptic structural protein expression and disrupted fear conditioning recall.G 蛋白偶联受体 75 缺失的小鼠表现出突触前结构蛋白表达改变和恐惧条件反射记忆缺失。
J Neurochem. 2023 Jun;165(6):827-841. doi: 10.1111/jnc.15818. Epub 2023 Apr 21.
6
Gpr75-deficient mice are protected from high-fat diet-induced obesity.Gpr75 缺陷型小鼠可预防高脂饮食诱导的肥胖。
Obesity (Silver Spring). 2023 Apr;31(4):1024-1037. doi: 10.1002/oby.23692. Epub 2023 Feb 28.
7
Mice Lacking are Hypophagic and Thin.缺乏（某种物质）的小鼠摄食量减少且体型消瘦。 （原句中“Lacking”后缺少关键信息，以上译文为补充完整关键信息后的内容）
Diabetes Metab Syndr Obes. 2022 Jan 5;15:45-58. doi: 10.2147/DMSO.S342799. eCollection 2022.
8
Sequencing of 640,000 exomes identifies variants associated with protection from obesity.对 64 万外显子组进行测序，确定了与肥胖保护相关的变异。
Science. 2021 Jul 2;373(6550). doi: 10.1126/science.abf8683.
9
Constitutive G protein coupling profiles of understudied orphan GPCRs.研究较少的孤儿 GPCR 的组成型 G 蛋白偶联特征。
PLoS One. 2021 Apr 22;16(4):e0247743. doi: 10.1371/journal.pone.0247743. eCollection 2021.
10
Subcellular localization of MC4R with ADCY3 at neuronal primary cilia underlies a common pathway for genetic predisposition to obesity.MC4R 与 ADCY3 在神经元初级纤毛中的亚细胞定位为肥胖遗传易感性的共同途径奠定了基础。
Nat Genet. 2018 Feb;50(2):180-185. doi: 10.1038/s41588-017-0020-9. Epub 2018 Jan 8.