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本文引用的文献

1
Iron dysregulation in COVID-19 and reciprocal evolution of SARS-CoV-2: Natura nihil frustra facit.新冠病毒感染中的铁代谢失调与 SARS-CoV-2 的相互进化：自然不会徒劳无功。
J Cell Biochem. 2022 Mar;123(3):601-619. doi: 10.1002/jcb.30207. Epub 2022 Jan 8.
2
Serum ferritin levels in inflammation: a retrospective comparative analysis between COVID-19 and emergency surgical non-COVID-19 patients.血清铁蛋白水平与炎症：COVID-19 与急诊非 COVID-19 手术患者的回顾性对比分析。
World J Emerg Surg. 2021 Mar 8;16(1):9. doi: 10.1186/s13017-021-00354-3.
3
Hepcidin is a friend rather than a foe in COVID19-induced complications.在 COVID19 引发的并发症中，铁调素是朋友而非敌人。
Acta Biomed. 2020 Nov 5;91(4):e2020138. doi: 10.23750/abm.v91i4.10768.
4
Hepcidin levels predict Covid-19 severity and mortality in a cohort of hospitalized Italian patients.在一组意大利住院患者中，铁调素水平可预测新冠病毒疾病的严重程度和死亡率。
Am J Hematol. 2021 Jan;96(1):E32-E35. doi: 10.1002/ajh.26027. Epub 2020 Nov 3.
5
Increased Serum Levels of Hepcidin and Ferritin Are Associated with Severity of COVID-19.血清铁调素和铁蛋白水平升高与 COVID-19 严重程度相关。
Med Sci Monit. 2020 Sep 26;26:e926178. doi: 10.12659/MSM.926178.
6
Fibrinolysis Shutdown in COVID-19-Infected Patients Can Result from Iron-Induced Stabilization of Fibril Clots.新冠病毒感染患者的纤维蛋白溶解停止可能是由铁诱导的纤维凝块稳定所致。
J Am Coll Surg. 2020 Nov;231(5):607-608. doi: 10.1016/j.jamcollsurg.2020.08.170. Epub 2020 Sep 22.
7
High D dimers and low global fibrinolysis coexist in COVID19 patients: what is going on in there?在 COVID-19 患者中同时存在高 D 二聚体和低整体纤维蛋白溶解：这是怎么回事？
J Thromb Thrombolysis. 2021 Feb;51(2):308-312. doi: 10.1007/s11239-020-02226-0. Epub 2020 Jul 15.
8
Differences in morphology of fibrin clots induced with thrombin and ferric ions and its pathophysiological consequences.凝血酶和铁离子诱导的纤维蛋白凝块形态学的差异及其病理生理学后果。
Heart Lung Circ. 2013 Jun;22(6):447-9. doi: 10.1016/j.hlc.2012.10.010. Epub 2012 Dec 7.
9
Iron and iron-related proteins in the lower respiratory tract of patients with acute respiratory distress syndrome.急性呼吸窘迫综合征患者下呼吸道中的铁及铁相关蛋白
Crit Care Med. 2003 Feb;31(2):395-400. doi: 10.1097/01.CCM.0000050284.35609.97.

现在是否是关注 COVID-19 引发的炎症引发的铁介导病理学的时候了？

Is it a high time to focus on iron-mediated pathology initiated by COVID-induced inflammation?

机构信息

a:1:{s:5:"en_US";s:81:"N.M.Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Moscow";}.

出版信息

Acta Biomed. 2022 May 11;93(2):e2022229. doi: 10.23750/abm.v93i2.13165.

DOI:10.23750/abm.v93i2.13165
PMID:35545994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9171865/
Abstract

A comment to paper published in the current issue by Duca et al (Acta Biomed 2022; Vol. 93, N. 2: e2022057 - DOI 10.23750/abm.v93i2.12937 - https://mattioli1885journals.com/index.php/actabiomedica/article/view/12937). The paper demonstrated a link between deregulated iron homeostasis and hyperinflammation in nontreated COVID-19 patients. Iron homeostasis links two generally accepted COVID-initiated pathological events: hyperinflammation and abnormal fibrin clotting. Intensive research is needed to look for the ways how to support and recover FeH in COVID infected patients.

摘要

对 Duca 等人在本期发表的论文的评论（《生物医学学报》2022 年；第 93 卷，第 2 期：e2022057- DOI 10.23750/abm.v93i2.12937- https://mattioli1885journals.com/index.php/actabiomedica/article/view/12937）。该论文证明了铁稳态失调与未经治疗的 COVID-19 患者的过度炎症之间存在关联。铁稳态将两个普遍公认的 COVID 引发的病理事件联系起来：过度炎症和异常纤维蛋白凝结。需要进行深入研究，以寻找支持和恢复 COVID 感染患者铁稳态的方法。