在衰老的内皮细胞中,SARS-CoV-2的吸收和炎症反应由BSG/VEGFR2通路调节
Yuya Sakurai1,2, Yoichiro Fujioka3,4, Nako Maishi1
1Vascular Biology and Molecular Pathology, Faculty and Graduate School of Dental Medicine, Hokkaido University, Sapporo 060-8586, Japan.
衰老的内皮细胞 (ECs) 通过内细胞分裂 (endocytosis) 增加了SARS-CoV-2的吸收,引发了炎症和血管功能障碍. 针对这种增强的内细胞分裂可能为老年人严重的COVID-19提供治疗策略.
科学领域:
- 血管生物学 血管生物学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 衰老是严重COVID-19的重要危险因素,通常涉及血管内皮功能障碍.
- 血管内皮细胞 (ECs) 可能对SARS-CoV-2敏感,但病毒进入的确切机制尚不清楚.
研究的目的:
- 研究衰老EC的内细胞能力及其在SARS-CoV-2吸收中的作用.
- 阐明SARS-CoV-2进入老年EC的分子机制.
主要方法:
- 利用了严重的COVID-19的老鼠模型.
- 在老化的EC中评估了内细胞容量和病毒吸收.
- 研究了Basigin和血管内皮生长因子 (VEGF) 信号传递的作用.
主要成果:
- 衰老的EC表现出增加的内细胞活动和显著的SARS-CoV-2吸收.
- 这种吸收激活了核因子-kappa B (NF-κB) 途径,导致炎症反应.
- 通过激活细胞内VEGF信号传递,Basigin被发现可以增强衰老的EC中的内细胞分裂.
结论:
- 欧冠衰老与SARS-CoV-2内细胞增多和随后的血管内皮功能障碍有关.
- 准EC衰老和Basigin介导途径为老年人严重的COVID-19提供了潜在的治疗途径.
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