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IL1β 通过 p38 MAPK-GATA2 轴促进 TMPRSS2 表达和 SARS-CoV-2 细胞进入。

IL1β Promotes TMPRSS2 Expression and SARS-CoV-2 Cell Entry Through the p38 MAPK-GATA2 Axis.

机构信息

Department of Biomedical Sciences, University of Padova, Padova, Italy.

Istituto di Ricerca Pediatrica (IRP), Fondazione Città della Speranza, Padova, Italy.

出版信息

Front Immunol. 2021 Dec 7;12:781352. doi: 10.3389/fimmu.2021.781352. eCollection 2021.

Abstract

After the outburst of the SARS-CoV-2 pandemic, a worldwide research effort has led to the uncovering of many aspects of the COVID-19, among which we can count the outstanding role played by inflammatory cytokine milieu in the disease progression. Despite that, molecular mechanisms that regulate SARS-CoV-2 pathogenesis are still almost unidentified. In this study, we investigated whether the pro-inflammatory milieu of the host affects the susceptibility of SARS-CoV-2 infection by modulating and expression. Our results indicated that the host inflammatory milieu favors SARS-CoV-2 infection by directly increasing TMPRSS2 expression. We unveiled the molecular mechanism that regulates this process and that can be therapeutically advantageously targeted.

摘要

在 SARS-CoV-2 大流行爆发后,全球范围内的研究努力揭示了 COVID-19 的许多方面,其中包括炎症细胞因子在疾病进展中发挥的突出作用。尽管如此,调节 SARS-CoV-2 发病机制的分子机制仍几乎未被识别。在这项研究中,我们通过调节 和 表达,研究了宿主的促炎环境是否通过影响 SARS-CoV-2 感染的易感性。我们的结果表明,宿主炎症环境通过直接增加 TMPRSS2 表达,有利于 SARS-CoV-2 感染。我们揭示了调节这一过程的分子机制,该机制可能具有治疗优势。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8ae/8691651/4816044749b9/fimmu-12-781352-g001.jpg

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