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髓状GPSM1通过控制单细胞和巨细胞的激活和化学反应来调节动脉样硬化的进展

Yuemei Zhang¹, Yuxin Cao¹, Yongxin Sun²

¹Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai 200233, China.

Proceedings of the National Academy of Sciences of the United States of America

|November 26, 2025

概括

G-蛋白信号调节器1 (GPSM1) 通过促进单细胞激活和炎症来驱动动动脉硬化. 在临床前模型中抑制GPSM1减少了疾病的进展,这表明GPSM1是动脉样硬化的潜在治疗标.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
免疫学免疫学免疫学

背景情况:

动脉样硬化涉及单细胞激活和巨细胞透到血管壁.
调节这些动脉动脉生成过程的机制尚未完全理解.

研究的目的:

研究G蛋白信号调节器1 (GPSM1) 在动脉样硬化的发展中的作用.
阐明GPSM1影响动脉生成的分子机制.

主要方法:

评估了小鼠和人类动脉样硬化病变中的GPSM1表达.
利用了骨髓细胞特异的GPSM1淘汰和过度表达的小鼠模型.
研究的信号通路包括p38/ERK MAPK和cAMP/PKA/KLF4/PMP22轴.
评估了针对GPSM1和PMP22的治疗干预措施.

主要成果:

在动脉样硬化期间,GPSM1表达在损伤性巨细胞中被上调.
骨髓体GPSM1切除保护于动脉样硬化和大动脉炎症.
通过cAMP/PKA/KLF4/PMP22调节的p38/ERK MAPK通路,GPSM1缺乏抑制了单细胞激活.
针对GPSM1或PMP22在小鼠模型中改善了动脉样硬化.

结论:

GPSM1是动脉样硬化发展的关键调节者.
GPSM1促进单细胞激活和动脉样硬化斑块中的炎症反应.
向GPSM1代表了对动脉样硬化的潜在治疗策略.

关键词:

这是一个GPSM1GPSM1 动脉样硬化动脉样硬化化学反应的化学作用.巨细胞是什么?巨细胞是什么?单细胞 (Monocytes) 是一种单细胞.

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