在COVID-19后和IPF中MMP-2和MMP-9的失调:与全身炎症和内皮功能障碍的相关性
Olga V Balan1, Irina E Malysheva1, Ella L Tikhonovich2
1Centre for Biomedical Research, Karelian Research Centre of the Russian Academy of Sciences (KarRC RAS), 185910 Petrozavodsk, Russia.
Journal of clinical medicine
|January 28, 2026
概括
后COVID-19肺纤维化涉及持续的矩阵金属蛋白酶 (MMP) 失调,持续的炎症和晚期发作的内皮功能障碍. 这些因素创造了一个自我强化的循环,类似于异常性肺纤维化,表明共享的纤维化途径.
科学领域:
- 肺部医学 肺部医学
- 免疫学 免疫学 免疫学
- 心血管生物学 心血管生物学
背景情况:
- 后COVID-19肺纤维化 (PCPF) 与异常性肺纤维化 (IPF) 有病理相似之处.
- 在康复期的COVID-19患者中调查持续的分子通路失调至关重要.
研究的目的:
- 检查PCPF中的矩阵金属蛋白酶 (MMP) -2和MMP-9失调.
- 评估MMPs,全身炎症和内皮功能障碍之间的关系.
- 为了比较PCPF患者与异形性肺纤维化 (IPF) 和健康对照中的这些标志物.
主要方法:
- 86名康复COVID-19患者的前性观察研究 (PCPF与无纤维化).
- 通过qRT-PCR和ELISA量化MMP-2,MMP-9,细胞因子 (TNF-α,IL-6) 和内皮标记物 (ET-1,粘附分子).
- 与健康的捐赠者和IPF患者进行比较.
主要成果:
- 在所有COVID-19后患者中,MMP-2和MMP-9的持续升高,在PCPF组更高,类似于IPF.
- 12个月后,PCPF患者表现出持续的炎症和严重的晚期内皮功能障碍 (增加ET-1,粘附分子).
- 在MMPs,ET-1和sICAM-1之间发现了正相关性.
结论:
- PCPF的发展与持续的MMP失调,未解决的炎症和晚期内皮功能障碍有关.
- 这些因素可能形成一个自我强化的病原性循环.
- 在PCPF中观察到的系统性特征反映了IPF,表明共享的纤维细胞路径和潜在的治疗点.
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