与MAPT结合的CCL18通过抑制自和触发细胞衰老来促进慢性阻塞性肺病
Hongbo Chen1, Lina Wang1, Jie Liu1
1Department Respiratory Medicine, Anning First People's Hospital Affiliated to Kunming University of Science and Technology, Kunming 650302, China.
Tissue & cell
|February 28, 2026
概括
CCL18上调驱动慢性阻塞性肺病 (COPD) 通过抑制自和通过MAPT促进细胞衰老. 减少CCL18可能提供一种新的COPD治疗方法.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 分子病理学分子病理学
背景情况:
- 化学基因CCL18在慢性阻塞性肺病 (COPD) 中升高.
- 目前尚不完全了解CCL18在COPD病原体中的确切作用.
- 研究CCL18在MAPT介导的自和衰老中的参与至关重要.
研究的目的:
- 为了阐明CCL18在COPD发病过程中的作用.
- 为了确定CCL18是否通过MAPT调节自和细胞衰老.
- 探索CCL18作为COPD潜在的治疗点.
主要方法:
- 已建立的COPD动物和细胞模型使用香烟烟雾 (CS) 和提取物 (CSE).
- 使用RT-qPCR,西部斑点,SA-β-Gal染色,流细胞计,ELISA和H&E染色.
- 进行了CCL18的淘汰实验,以评估下游效应.
主要成果:
- 在COPD样本和模型中,CCL18表达显著增加.
- CCL18 Knockdown 降低了衰老标志物 (VEGF,MMP1,p27,p16,p21) 和炎症性细胞因子 (IL-6,IL-1β,TNF-α) 以及ROS.
- CCL18 Knockdown增强了自标志物 (Lamin B1,LC3II/I,Beclin1) 和缓解了肺损伤,延缓了COPD的进展.
结论:
- CCL18通过通过MAPT上调抑制自,从而促进COPD的发展,从而导致细胞衰老.
- 针对CCL18的定向下调是一种有前途的COPD治疗策略.
- 了解CCL18-MAPT-自-衰老轴是治疗COPD的关键.
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