纵向的ARDS和败血症炎症表型的多原子特征确定了与死亡率相关的关键途径
Narges Alipanah-Lechner1, Lucile Neyton1, Pratik Sinha2
1Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco; USA.
medRxiv : the preprint server for health sciences
|September 18, 2025
概括
患有急性呼吸窘迫综合征 (ARDS) 和败血症的重症患者具有不同的炎症表型. 多omics分析揭示了与这些表型和患者死亡率相关的特定分子特征,提供了潜在的治疗点.
科学领域:
- 关键护理医学 关键护理医学
- 分子生物学分子生物学
- 系统生物学 系统生物学
背景情况:
- 患有急性呼吸窘迫综合征 (ARDS) 和败血症的重症患者表现出不同的炎症反应和临床结果.
- 这些独特的炎症表型的分子基础在很大程度上是未知的.
- 之前的研究表明,这些表型与代谢差异之间存在联系.
研究的目的:
- 在ARDS患者中研究超炎性和低炎性表型之间的代谢和转录学差异.
- 通过整合性多组学分析,识别与这些表型内的死亡率相关的分子机制.
- 为了验证一个独立队列的严重病症败血症患者的发现.
主要方法:
- 在ROSE试验中,从ARDS患者的血液样本中进行了综合性多组学分析 (代谢学和转录学).
- 识别与炎症表型和死亡率相关的分子特征.
- 在一个独立的败血症患者队列 (EARLI) 中验证已识别的签名.
主要成果:
- 确定了与高炎症表型和死亡率相关的三个分子特征:先天性免疫激活/糖解,肝脏/免疫功能障碍/脂肪酸氧化障碍,干扰素抑制/线粒体呼吸变化.
- 与死亡率相关的第四个特征,独立于炎症表型,涉及氧化还原功能障碍和细胞增殖.
- 在每个炎症表型中发现了与死亡相关的显著分子通路,并在队列中验证.
结论:
- 在ARDS和败血症中,明显的分子机制是超炎症和低炎症表型的基础.
- 特定的分子特征与重症患者的死亡率有关.
- 这些发现突出了重症患者精准医学的潜在治疗目标.
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