NOTCH signaling in COVID-19: a central hub controlling genes, proteins, and cells that mediate SARS-CoV-2 entry, the inflammatory response, and lung regeneration.
NOTCH signaling in COVID-19: a central hub controlling genes, proteins, and cells that mediate SARS-CoV-2 entry, the inflammatory response, and lung regeneration.
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DOI：
10.3389/fcimb.2022.928704
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发表时间：
2022
影响因子：
5.7
通讯作者：
中科院分区：
文献类型：
--
作者：
在受感染个体的肺部，严重急性呼吸综合征冠状病毒2 （SARS-CoV-2）诱导的下游分子信号通路尚不完全清楚。在这里，我们描述并检查了NOTCH可能代表2019冠状病毒病（COVID-19）肺部感染中心信号轴的模型的预测。一个涉及NOTCH信号、furin、ADAM17和ACE2的通路可能能够增加SARS-CoV-2病毒的进入和感染。NOTCH信号还可以上调IL-6和促炎介质在COVID-19中诱导的过度激活。此外，如果NOTCH信号不能正常下调并保持升高，肺愈合过程中的气道再生就会受到抑制——这一过程可能在COVID-19中起作用。随着特定的NOTCH抑制剂药物的开发和其他疾病的临床试验正在进行，如果这些药物可能应用于COVID-19患者，NOTCH在所有这些过程中对感染和愈合至关重要的作用值得考虑。
In the lungs of infected individuals, the downstream molecular signaling pathways induced by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) are incompletely understood. Here, we describe and examine predictions of a model in which NOTCH may represent a central signaling axis in lung infection in Coronavirus Disease 2019 (COVID-19). A pathway involving NOTCH signaling, furin, ADAM17, and ACE2 may be capable of increasing SARS-CoV-2 viral entry and infection. NOTCH signaling can also upregulate IL-6 and pro-inflammatory mediators induced to hyperactivation in COVID-19. Furthermore, if NOTCH signaling fails to turn down properly and stays elevated, airway regeneration during lung healing can be inhibited—a process that may be at play in COVID-19. With specific NOTCH inhibitor drugs in development and clinical trials for other diseases being conducted, the roles of NOTCH in all of these processes central to both infection and healing merit contemplation if such drugs might be applied to COVID-19 patients.
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