SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway.

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Stress & Chaperones Pub Date : 2023-11-01 Epub Date: 2023-10-05 DOI:10.1007/s12192-023-01379-0

Rabab S Hamad, Hayder M Al-Kuraishy, Athanasios Alexiou, Marios Papadakis, Eman A Ahmed, Hebatallah M Saad, Gaber El-Saber Batiha

{"title":"SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway.","authors":"Rabab S Hamad, Hayder M Al-Kuraishy, Athanasios Alexiou, Marios Papadakis, Eman A Ahmed, Hebatallah M Saad, Gaber El-Saber Batiha","doi":"10.1007/s12192-023-01379-0","DOIUrl":null,"url":null,"abstract":"<p><p>Coronavirus disease 2019 (COVID-19) is a recent pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) leading to pulmonary and extra-pulmonary manifestations due to the development of oxidative stress (OS) and hyperinflammation. The underlying cause for OS and hyperinflammation in COVID-19 may be related to the inhibition of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of antioxidative responses and cellular homeostasis. The Nrf2 pathway inhibits the expression of pro-inflammatory cytokines and the development of cytokine storm and OS in COVID-19. Nrf2 activators can attenuate endothelial dysfunction (ED), renin-angiotensin system (RAS) dysregulation, immune thrombosis, and coagulopathy. Hence, this review aimed to reveal the potential role of the Nrf2 pathway and its activators in the management of COVID-19. As well, we tried to revise the mechanistic role of the Nrf2 pathway in COVID-19.</p>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":" ","pages":"657-673"},"PeriodicalIF":3.3000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10746631/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Stress & Chaperones","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12192-023-01379-0","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/10/5 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Coronavirus disease 2019 (COVID-19) is a recent pandemic caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) leading to pulmonary and extra-pulmonary manifestations due to the development of oxidative stress (OS) and hyperinflammation. The underlying cause for OS and hyperinflammation in COVID-19 may be related to the inhibition of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of antioxidative responses and cellular homeostasis. The Nrf2 pathway inhibits the expression of pro-inflammatory cytokines and the development of cytokine storm and OS in COVID-19. Nrf2 activators can attenuate endothelial dysfunction (ED), renin-angiotensin system (RAS) dysregulation, immune thrombosis, and coagulopathy. Hence, this review aimed to reveal the potential role of the Nrf2 pathway and its activators in the management of COVID-19. As well, we tried to revise the mechanistic role of the Nrf2 pathway in COVID-19.

Abstract Image

查看原文本刊更多论文

严重急性呼吸系统综合征冠状病毒2型感染和核因子-红细胞2型相关因子2（Nrf2）通路失调。

2019冠状病毒病（新冠肺炎）是一种新型严重急性呼吸综合征冠状病毒2（SARS‑CoV‑2）引起的近期大流行，由于氧化应激（OS）和过度炎症的发展，导致肺部和肺外表现。新冠肺炎OS和过度炎症的根本原因可能与核因子红细胞2型相关因子2（Nrf2）的抑制有关，Nrf2是抗氧化反应和细胞稳态的主要调节因子。Nrf2通路抑制新冠肺炎中促炎细胞因子的表达以及细胞因子风暴和OS的发展。Nrf2激活剂可以减轻内皮功能障碍（ED）、肾素-血管紧张素系统（RAS）失调、免疫血栓形成和凝血障碍。因此，本综述旨在揭示Nrf2通路及其激活剂在新冠肺炎管理中的潜在作用。此外，我们还试图修正Nrf2通路在新冠肺炎中的机制作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cell Stress & Chaperones 生物-细胞生物学

CiteScore

7.60

自引率

2.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.