巨细胞衍生的S100A9通过通过STAT3激活扰乱线粒体质量控制来促进糖尿病心肌病
Shengqi Huo1,2, Moran Wang1, Min Du1
1Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, Hubei, China, 430030.
International journal of biological sciences
|May 19, 2025
概括
巨细胞衍生的S100A9通过损害线粒体功能驱动糖尿病心肌病. 阻止S100A9或其通路可缓解心脏功能障碍,为糖尿病心脏病提供潜在的治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 代谢性疾病研究研究
背景情况:
- 糖尿病心肌病 (DCM) 涉及复杂的巨细胞-心肌细胞相互作用.
- 在DCM中,S100A9等炎症媒介的特殊作用需要进一步研究.
研究的目的:
- 调查S100A9在糖尿病心肌病中的作用.
- 探索S100A9作为DCM的潜在治疗点.
主要方法:
- 单细胞RNA测序以识别糖尿病心脏中的S100A9.
- 在体内研究使用S100A9抑制 (paquinimod),巨枯竭 (clodronate) 和巨特定的S100A9淘汰赛小鼠.
- 对心脏功能,炎症,线粒体动态和STAT3信号的分析.
主要成果:
- 在糖尿病心脏中,S100A9在心肌细胞和巨细胞上调.
- 在糖尿病小鼠中观察到F4/80+CCR2+S100A9+巨细胞的增加.
- S100A9阻塞或耗尽改善心脏功能障碍和炎症.
- 宏细胞特异性S100A9淘汰抑制了DCM,线粒体功能障碍和STAT3激活.
结论:
- 巨衍生的S100A9是DCM中线粒体功能障碍的关键调解者.
- 针对S100A9是一个有前途的治疗策略,用于糖尿病心肌病.
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