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Neuropilin-1: A feasible link between liver pathologies and COVID-19
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has a tremendous impact on the health of millions of people worldwide. Unfortunately, those suffering from previous pathological conditions are more vulnerable and tend to develop more severe disease upon infection with the ne...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240058/ https://www.ncbi.nlm.nih.gov/pubmed/34239266 http://dx.doi.org/10.3748/wjg.v27.i24.3516 |
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author | Benedicto, Aitor García-Kamiruaga, Iñigo Arteta, Beatriz |
author_facet | Benedicto, Aitor García-Kamiruaga, Iñigo Arteta, Beatriz |
author_sort | Benedicto, Aitor |
collection | PubMed |
description | The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has a tremendous impact on the health of millions of people worldwide. Unfortunately, those suffering from previous pathological conditions are more vulnerable and tend to develop more severe disease upon infection with the new SARS-CoV-2. This coronavirus interacts with the angiotensin-converting enzyme 2 receptor to invade the cells. Recently, another receptor, neuropilin-1 (NRP-1), has been reported to amplify the viral infection. Interestingly, NRP-1 is expressed in nonparenchymal liver cells and is related to and upregulated in a wide variety of liver-related pathologies. It has been observed that SARS-CoV-2 infection promotes liver injury through several pathways that may be influenced by the previous pathological status of the patient and liver expression of NRP-1. Moreover, coronavirus disease 2019 causes an inflammatory cascade called cytokine storm in patients with severe disease. This cytokine storm may influence liver sinusoidal-cell phenotype, facilitating viral invasion. In this review, the shreds of evidence linking NRP-1 with liver pathologies such as hepatocellular carcinoma, liver fibrosis, nonalcoholic fatty liver disease and inflammatory disorders are discussed in the context of SARS-CoV-2 infection. In addition, the involvement of the infection-related cytokine storm in NRP-1 overexpression and the subsequent increased risk of SARS-CoV-2 infection are also analyzed. This review aims to shed some light on the involvement of liver NRP-1 during SARS-CoV-2 infection and emphasizes the possible involvement this receptor with the observed liver damage. |
format | Online Article Text |
id | pubmed-8240058 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-82400582021-07-07 Neuropilin-1: A feasible link between liver pathologies and COVID-19 Benedicto, Aitor García-Kamiruaga, Iñigo Arteta, Beatriz World J Gastroenterol Review The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has a tremendous impact on the health of millions of people worldwide. Unfortunately, those suffering from previous pathological conditions are more vulnerable and tend to develop more severe disease upon infection with the new SARS-CoV-2. This coronavirus interacts with the angiotensin-converting enzyme 2 receptor to invade the cells. Recently, another receptor, neuropilin-1 (NRP-1), has been reported to amplify the viral infection. Interestingly, NRP-1 is expressed in nonparenchymal liver cells and is related to and upregulated in a wide variety of liver-related pathologies. It has been observed that SARS-CoV-2 infection promotes liver injury through several pathways that may be influenced by the previous pathological status of the patient and liver expression of NRP-1. Moreover, coronavirus disease 2019 causes an inflammatory cascade called cytokine storm in patients with severe disease. This cytokine storm may influence liver sinusoidal-cell phenotype, facilitating viral invasion. In this review, the shreds of evidence linking NRP-1 with liver pathologies such as hepatocellular carcinoma, liver fibrosis, nonalcoholic fatty liver disease and inflammatory disorders are discussed in the context of SARS-CoV-2 infection. In addition, the involvement of the infection-related cytokine storm in NRP-1 overexpression and the subsequent increased risk of SARS-CoV-2 infection are also analyzed. This review aims to shed some light on the involvement of liver NRP-1 during SARS-CoV-2 infection and emphasizes the possible involvement this receptor with the observed liver damage. Baishideng Publishing Group Inc 2021-06-28 2021-06-28 /pmc/articles/PMC8240058/ /pubmed/34239266 http://dx.doi.org/10.3748/wjg.v27.i24.3516 Text en ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Review Benedicto, Aitor García-Kamiruaga, Iñigo Arteta, Beatriz Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title | Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title_full | Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title_fullStr | Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title_full_unstemmed | Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title_short | Neuropilin-1: A feasible link between liver pathologies and COVID-19 |
title_sort | neuropilin-1: a feasible link between liver pathologies and covid-19 |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240058/ https://www.ncbi.nlm.nih.gov/pubmed/34239266 http://dx.doi.org/10.3748/wjg.v27.i24.3516 |
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