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COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis

COVID-19 has an extensive impact on Homo sapiens globally. Patients with COVID-19 are at an increased risk of developing pulmonary fibrosis. A previous study identified that myofibroblasts could be derived from pulmonary endothelial lineage cells as an important cell source that contributes to pulmo...

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Autores principales: Wu, Xiuju, Zhang, Daoqin, Boström, Kristina I., Yao, Yucheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10380846/
https://www.ncbi.nlm.nih.gov/pubmed/37511258
http://dx.doi.org/10.3390/ijms241411500
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author Wu, Xiuju
Zhang, Daoqin
Boström, Kristina I.
Yao, Yucheng
author_facet Wu, Xiuju
Zhang, Daoqin
Boström, Kristina I.
Yao, Yucheng
author_sort Wu, Xiuju
collection PubMed
description COVID-19 has an extensive impact on Homo sapiens globally. Patients with COVID-19 are at an increased risk of developing pulmonary fibrosis. A previous study identified that myofibroblasts could be derived from pulmonary endothelial lineage cells as an important cell source that contributes to pulmonary fibrosis. Here, we analyzed publicly available data and showed that COVID-19 infection drove endothelial lineage cells towards myofibroblasts in pulmonary fibrosis of patients with COVID-19. We also discovered a similar differentiation trajectory in mouse lungs after viral infection. The results suggest that COVID-19 infection leads to the development of pulmonary fibrosis partly through the activation of endothelial cell (EC)-like myofibroblasts.
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spelling pubmed-103808462023-07-29 COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis Wu, Xiuju Zhang, Daoqin Boström, Kristina I. Yao, Yucheng Int J Mol Sci Communication COVID-19 has an extensive impact on Homo sapiens globally. Patients with COVID-19 are at an increased risk of developing pulmonary fibrosis. A previous study identified that myofibroblasts could be derived from pulmonary endothelial lineage cells as an important cell source that contributes to pulmonary fibrosis. Here, we analyzed publicly available data and showed that COVID-19 infection drove endothelial lineage cells towards myofibroblasts in pulmonary fibrosis of patients with COVID-19. We also discovered a similar differentiation trajectory in mouse lungs after viral infection. The results suggest that COVID-19 infection leads to the development of pulmonary fibrosis partly through the activation of endothelial cell (EC)-like myofibroblasts. MDPI 2023-07-15 /pmc/articles/PMC10380846/ /pubmed/37511258 http://dx.doi.org/10.3390/ijms241411500 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Communication
Wu, Xiuju
Zhang, Daoqin
Boström, Kristina I.
Yao, Yucheng
COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title_full COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title_fullStr COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title_full_unstemmed COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title_short COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis
title_sort covid-19 infection may drive ec-like myofibroblasts towards myofibroblasts to contribute to pulmonary fibrosis
topic Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10380846/
https://www.ncbi.nlm.nih.gov/pubmed/37511258
http://dx.doi.org/10.3390/ijms241411500
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