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在不可解决的COVID-19中解码纤维化:神经质特异性HIF1A删除的作用

Kemly Philip¹, Hannah P Thompson¹, Scott D Collum¹

¹Department of Biochemistry and Molecular Biology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, United States.

American journal of physiology. Cell physiology

|October 25, 2025

概括

肌性缺氧诱导因子1A (HIF1A) 表达的减少加剧了严重的COVID-19中的肺损伤和纤维化. 向HIF1A可能会预防渐进的病毒后肺纤维化,但由于潜在的纤维化结果,需要仔细考虑.

科学领域:

肺部医学肺部医学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

病毒性肺部感染,特别是COVID-19,可以导致严重的肺纤维化.
无法解决的 (NR) -COVID-19呈现为突发性纤维化肺损伤,有时需要进行肺移植.
驱动这种快速纤维化的机制,特别是缺氧的作用,仍然不完全理解.

研究的目的:

调查缺氧反应,特别是缺氧诱导因子1A (HIF1A) 在严重COVID-19相关肺纤维化病原体中的作用.
为了确定骨髓细胞中减少的HIF1A是否有助于加剧肺损伤.

主要方法:

从重症COVID-19患者的肺组织中分析HIF1A表达,包括NR-COVID-19.
使用了特定于骨髓细胞的HIF1A淘汰赛小鼠 (溶酶M Cre促进剂).
给小鼠慢性低剂量布莱奥米辛,以诱导肺损伤和纤维化.

主要成果:

严重的COVID-19患者,包括NR-COVID-19,尽管整体HIF1A和ADORA2B增加,但巨细胞中的HIF1A表达减少.
骨髓特异性HIF1A淘汰赛小鼠在接受白胺治疗后表现出恶化的肺炎和纤维化.
淘汰赛小鼠中增加的肺损伤与减少的替代激活的巨细胞标记物有关,反映了NR-COVID-19肺部的发现.

结论:

减少的骨髓质HIF1A是一种潜在的机制,在严重的COVID-19中导致肺部损伤和快速纤维化.
HIF1A稳定剂可能是预防后病毒性肺纤维化的治疗策略.
需要谨慎使用,因为慢性HIF1A激活也可能促进纤维化.

关键词:

在 COVID-19 疫情中,这就是SARS-COV2病毒.氨酸 (Adenosine) 是一种氨酸.肺部纤维化肺部纤维化巨细胞是什么?巨细胞是什么?

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