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作为一种治疗策略，针对 SARS-CoV-2 诱导的细胞因子风暴对 IRAK 酶进行调节。

Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm.

机构信息

Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, The Hashemite University, Zarqa, 13133, Jordan.

Department of Basic Medical Sciences, Faculty of Medicine, Al-Balqa Applied University, As-Salt, Jordan.

出版信息

Clin Exp Med. 2023 Oct;23(6):2909-2923. doi: 10.1007/s10238-023-01064-7. Epub 2023 Apr 15.

DOI:10.1007/s10238-023-01064-7
PMID:37061574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10105542/
Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the current pandemic coronavirus disease 2019 (COVID-19). Dysregulated and excessive production of cytokines and chemokines, known as cytokine storm, is frequently seen in patients with severe COVID-19 disease and it can provoke a severe systematic inflammation in the patients. The IL-1R/TLRs/IRAKs signaling network is a key pathway in immune cells that plays a central role in regulating innate immunity and inflammatory responses via stimulating the expression and production of various proinflammatory molecules including cytokines. Modulation of IRAKs activity has been proposed to be a promising strategy in the treatment of inflammatory disorders. In this review, we highlight the biochemical properties of IRAKs and their role in regulating inflammatory molecular signaling pathways and discuss the potential targeting of IRAKs to suppress the SARS-CoV-2-induced cytokine storm in COVID-19 patients.

摘要

严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）是当前流行的 2019 年冠状病毒病（COVID-19）的病原体。在重症 COVID-19 患者中，经常观察到细胞因子和趋化因子的失调和过度产生，称为细胞因子风暴，这会引发患者的严重系统性炎症。IL-1R/TLRs/IRAKs 信号网络是免疫细胞中的关键途径，通过刺激包括细胞因子在内的各种促炎分子的表达和产生，在调节固有免疫和炎症反应中发挥核心作用。调节 IRAKs 的活性被认为是治疗炎症性疾病的一种有前途的策略。在这篇综述中，我们强调了 IRAKs 的生化特性及其在调节炎症分子信号通路中的作用，并讨论了靶向 IRAKs 以抑制 COVID-19 患者中 SARS-CoV-2 诱导的细胞因子风暴的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/2f8325aa2366/10238_2023_1064_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/094d3c8842d5/10238_2023_1064_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/3e15dea6651a/10238_2023_1064_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/bd30bdb2b1a1/10238_2023_1064_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/2f8325aa2366/10238_2023_1064_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/094d3c8842d5/10238_2023_1064_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/3e15dea6651a/10238_2023_1064_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/bd30bdb2b1a1/10238_2023_1064_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a4b/10105542/2f8325aa2366/10238_2023_1064_Fig4_HTML.jpg

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