烟草中的毒素通过铁灭菌诱导骨质疏松症
Zheng Jing1, Yuzhou Li1, He Zhang1
1Stomatological Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China; Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China.
Redox biology
|October 12, 2023
概括
吸烟会显著降低骨密度,因为它会导致骨髓中介细胞干细胞 (BMSCs) 的铁亡. 针对这种细胞死亡途径可以预防和治疗与吸烟有关的骨质疏松症.
科学领域:
- 生物医学科学 生物医学科学
- 细胞生物学 细胞生物学
- 骨质疏松症研究 骨质疏松症研究
背景情况:
- 烟草吸烟是骨质疏松症的已知危险因素,与骨髓中介性干细胞 (BMSC) 的活力和功能降低有关.
- 吸烟诱导BMSC功能障碍和骨质疏松症的精确分子机制在很大程度上仍然不清楚.
研究的目的:
- 研究由香烟烟雾提取物 (CSE) 诱导的BMSC功能障碍背后的特定机制.
- 探索铁质在吸烟相关的骨质疏松症中的作用,并评估潜在的治疗点.
主要方法:
- 对人类吸烟者和暴露于CSE的老鼠的骨矿物质密度 (BMD) 的分析.
- 在CSE暴露后评估大鼠BMSC (rBMSC) 功能和生存能力.
- 转录组分析以确定关键的细胞通路.
- 在体内研究,使用CSE暴露的老鼠中的铁和铁代抑制剂.
主要成果:
- 与非吸烟者相比,吸烟者表现出明显较低的股骨部 BMD.
- 在老鼠中,CSE暴露降低了BMD,并损害了rBMSC功能.
- 转录基因和表型数据表明,CSE治疗的rBMSCs中铁亡途径的显著激活.
- 在rBMSCs中,CSE诱导的铁致死涉及活性氧物种,AMPK信号传递,NCOA4介导的铁致死,铁积累和脂质过氧化.
- 抑制铁和铁因改善了CSE暴露的老鼠的BMD损失.
结论:
- 铁化是驱动BMSC功能障碍和吸烟相关骨质疏松症的骨损失的关键机制.
- 向BMSC中的铁亡途径是一个有希望的治疗策略,用于预防和治疗吸烟引起的骨损伤.
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