氧化压力是ME/CFS和长期COVID的共同特征
Vishnu Shankar1, Julie Wilhelmy2, Ellis J Curtis3,4
1Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305.
概括
长期COVID和ME/CFS共享了涉及淋巴细胞中氧化应激的潜在分子机制. 甲福明可以通过减少长期COVID患者的T细胞增殖来提供潜在的治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 代谢学 代谢学 代谢学
背景情况:
- 长期COVID (LC) 影响全球超过6500万,呈现类似于肌痛性脑筋炎/慢性疲劳综合征 (ME/CFS) 的症状.
- 这两种疾病都缺乏经批准的治疗方法和可靠的诊断标记,需要对它们的分子基础进行研究.
研究的目的:
- 研究健康对照组,ME/CFS和LC捐赠者之间的外周血液淋巴细胞的生物能和分子差异.
- 确定ME/CFS和LC的共享机制基础和潜在的治疗目标.
主要方法:
- 来自25个健康对照组,27个ME/CFS和20个LC捐赠者的周围血液淋巴细胞的分析.
- 利用流细胞计,RNA测序,质谱和系统化学.
- 评估了氧化应激标志物,活性氧物种 (ROS) 清除途径和线粒体功能.
主要成果:
- 两个ME/CFS和LC组都显示了淋巴细胞中氧化应激的升高,特别是在记忆子组中.
- 观察到ROS清除途径的失调,包括改变的谷氨水平和线粒体超氧化物失调酶.
- 鉴定了性别特异性的氧化还原通路变化,女性呈现较高的ROS和水平,男性呈现较高的脂质氧化损伤.
结论:
- 共享的分子机制,特别是氧化应激和氧化还原途径异常,是ME/CFS和LC表型的基础.
- 这些机制的性别特异性可能会影响疾病的表现和进展.
- 甲胺在减弱女性T细胞过度增殖方面表现出潜在的潜力,这表明它是LC的可能治疗剂.
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