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缺GPR108促进尿酸诱导的脏间歇性纤维化

Deping Xu¹, Ping Yang², Wei Song²

¹Department of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China; The Clinical Laboratory, the Second People's Hospital of Hefei, The Affiliated Hefei Hospital of Anhui Medical University, Hefei, China.

Cellular signalling

|September 14, 2025

概括

缺乏G蛋白结合受体108 (GPR108) 会使尿酸高的脏损伤恶化. 在慢性病中,GPR108可保护纤维化和炎症.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

purin代谢导致的慢性高尿血症有助于损伤,包括炎症和纤维化.
皮质-介质细胞过渡 (EMT) 是纤维化的一个关键过程.
G蛋白结合受体108 (GPR108) 是已知的消极调节炎症,但其在病中的作用尚不清楚.

研究的目的:

调查GPR108在高尿血症引起的慢性病 (CKD) 中的作用.
探索GPR108对纤维化,炎症和EMT的影响.

主要方法:

利用氨酸养的小鼠来模拟高尿血症诱导的脏病.
在实验室研究中使用来自Gpr108淘汰赛小鼠的初级培养管状上皮细胞.
评估纤维化,EMT标志物,细胞因子水平,TGF-β1和NF-κB激活.

主要成果:

缺乏Gpr108的小鼠表现出恶化的纤维化,EMT和增加的细胞因子水平.
缺少GPR108的初级管状上皮细胞对尿酸诱导的EMT表现出高度敏感.
在缺乏Gpr108的细胞中,尿酸暴露导致TGF-β1的产生增加和NF-κB的激活.

结论:

缺GPR108会加剧脏炎症和纤维化在高尿血症诱导的CKD.
GPR108通过抑制NF-κB驱动的EMT和TGF-β1信号传输,起到保护调节器的作用.
在CKD中,GPR108具有减轻脏间歇性纤维化的潜在治疗标.

关键词:

慢性脏疾病慢性脏疾病皮质 - 介质细胞过渡.在 GPR1088 中使用.超性血症 (hyperuricemia) 是一种疾病,脏间歇性纤维化脏间歇性纤维化尿酸是什么尿酸是什么

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