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NCOA4介导的铁蛋白自噬:新冠病毒发病机制中的一个有害元凶?

NCOA4-Mediated Ferritinophagy: A Vicious Culprit in COVID-19 Pathogenesis?

作者信息

Jia Fengju, Liu Hongxia, Kang Shan

机构信息

School of Nursing, Qingdao University, Qingdao, China.

Yantai Ludong Hospital (Shandong Provincial Hospital Group), Yantai, China.

出版信息

Front Mol Biosci. 2021 Dec 15;8:761793. doi: 10.3389/fmolb.2021.761793. eCollection 2021.

DOI:10.3389/fmolb.2021.761793
PMID:34977155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8714652/
Abstract

Coronavirus disease 2019 (COVID-19) is a global pandemic that has caused widespread loss of life. Notably, in this disease, severe inflammatory reactions characterized by cytokine storms are caused by severe acute respiratory syndrome coronavirus 2. The cytokine storms may promote hyper-ferritinemia which can further intensify the inflammation. Moreover, elevated ferritin levels trigger nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy, in which ferritin is degraded and iron is released. Excess iron released from ferritinophagy can promote ferroptosis and cellular damage. Therefore, we propose that NCOA4-mediated ferritinophagy can be targeted to limit the ferroptosis and prevent the multi-organ damage and severity in COVID-19 patients.

摘要

2019冠状病毒病(COVID-19)是一场导致广泛生命损失的全球大流行疾病。值得注意的是,在这种疾病中,严重急性呼吸综合征冠状病毒2会引发以细胞因子风暴为特征的严重炎症反应。细胞因子风暴可能会促进高铁蛋白血症,进而加剧炎症。此外,铁蛋白水平升高会触发核受体辅激活因子4(NCOA4)介导的铁蛋白自噬,即铁蛋白被降解并释放出铁。铁蛋白自噬释放的过量铁可促进铁死亡和细胞损伤。因此,我们提出可以靶向NCOA4介导的铁蛋白自噬来限制铁死亡,并预防COVID-19患者的多器官损伤和病情严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f8a/8714652/a9cb6db65d97/fmolb-08-761793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f8a/8714652/a9cb6db65d97/fmolb-08-761793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f8a/8714652/a9cb6db65d97/fmolb-08-761793-g001.jpg

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