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感应受体介导的巨细胞极化改善了自发高血压大鼠的心肌重塑

Jiaqi Zhao¹, Ning Lu², Yuanyuan Qu³

¹Key Laboratory of Education Ministry of Xinjiang Endemic and Ethnic Diseases, NHC Key Laboratory for Prevention and Treatment of Central Asia High Incidence Diseases, Department of Pathophysiology, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.

Experimental biology and medicine (Maywood, N.J.)

|May 8, 2024

概括

感应受体 (CaSR) 调节高血压中的炎症. 激活CaSR可以降低血压,并通过将巨细胞转移到抗炎状态来改善心脏功能.

科学领域:

心血管研究研究心血管研究
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

慢性炎症驱动着基本高血压 (EH) 的进展.
感应受体 (CaSR) 是炎症过程的关键媒介.
大细胞 (Mφs) 在炎症反应中起着至关重要的作用.

研究的目的:

研究CaSR在EH中的作用及其对心脏重塑的影响.
评估高血压条件下CaSR调制的治疗潜力.

主要方法:

使用自发高血压大鼠 (SHRs) 和巨细胞系RAW264.7.7.
使用R568 (CaSR阳性调节器) 和NPS2143 (CaSR阴性调节器).
评估血压,心脏功能,巨细胞极化和NLRP3炎症酶激活.

主要成果:

在SHR中,R568降低了血压,缓解了心脏缩和纤维化.
R568增加了心肌的CaSR和M2巨细胞 (M2Mφs),同时减少了M1巨细胞 (M1Mφs).
在体外,R568抑制了NLRP3炎症酶激活和RAW264.7细胞中的M1Mφ极化.

结论:

在老鼠中,降低CaSR会加剧高血压和心脏损伤.
通过抑制炎症和改善心脏重塑,CaSR调制为EH提供了潜在的治疗策略.

关键词:

在NLRP3炎症酶体中,NLRP3炎症感应的受体是感应的受体.基本高血压是什么意思巨细胞的两极分化改造改造改造改造改造改造

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