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作 者:Changyao Li Heng Liu Jingru Li Xinheng He Haoran Zhu Wei Fu H.Eric Xu
机构地区:[1]The CAS Key Laboratory of Receptor Research,Shanghai Institute of Materia Medica,Chinese Academy of Sciences,Shanghai,China [2]School of Life Science and Technology,ShanghaiTech University,Shanghai,China [3]Lingang Laboratory,Shanghai,China [4]School of Chinese Materia Medica,Nanjing University of Chinese Medicine,Nanjing,Jiangsu,China [5]University of Chinese Academy of Sciences,Beijing,China [6]School of Pharmacy,Fudan University,Shanghai,China
出 处:《Cell Research》2024年第8期594-596,共3页细胞研究(英文版)
基 金:supported by grants from CAS Strategic Priority Research Program(XDB37030103 to H.E.X.);Shanghai Municipal Science and Technology Major Project(2019SHZDZX02 to H.E.X.);Shanghai Municipal Science and Technology Major Project(H.E.X.);the National Natural Science Foundation of China(32130022,82121005);the Lingang Laboratory(LG-GG-202204-01 to H.E.X.);the National Key R&D Program of China(2022YFC2703105 to H.E.X.)。
摘 要:Dear Editor,Succinic acid,once considered merely a tricarboxylic acid cycle intermediate,1 has been recognized for its significant role in influencing mitochondrial reactive oxygen species homeostasis.2 This is largely mediated through the G protein-coupled succinate receptor(SUCR1,also known as GPR91),which has emerged as a vital link connecting metabolic status to a myriad of physiological and pathological processes.SUCR1 is intricately involved in the regulation of blood pressure,3 angiogenesis,4 inflammation,5 and has been implicated in the pathogenesis of liver fibrosis,6 hypertension,and rheumatic arthritis.6 These multifaceted roles highlight the receptor’s potential as a promising therapeutic target for a wide spectrum of diseases.However,the molecular mechanisms underlying SUCR1’s activation by various ligands and its subsequent interaction with the inhibitory G protein(Gi)have remained elusive,hindering our comprehensive understanding of its broad physiological significance and therapeutic potential.
关 键 词:CR1 ACTIVATION connecting
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