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The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis

The mortality rate of idiopathic pulmonary fibrosis (IPF) increases yearly due to ineffective treatment. Given that the lung is exposed to the external environment, it is likely that oxidative stress, especially the stimulation of DNA, would be of particular importance in pulmonary fibrosis. DNA dam...

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Autores principales: Zhu, Jiahui, Liu, Lexin, Ma, Xiaodi, Cao, Xinyu, Chen, Yu, Qu, Xiangping, Ji, Ming, Liu, Huijun, Liu, Chi, Qin, Xiaoqun, Xiang, Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687113/
https://www.ncbi.nlm.nih.gov/pubmed/36421478
http://dx.doi.org/10.3390/antiox11112292
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author Zhu, Jiahui
Liu, Lexin
Ma, Xiaodi
Cao, Xinyu
Chen, Yu
Qu, Xiangping
Ji, Ming
Liu, Huijun
Liu, Chi
Qin, Xiaoqun
Xiang, Yang
author_facet Zhu, Jiahui
Liu, Lexin
Ma, Xiaodi
Cao, Xinyu
Chen, Yu
Qu, Xiangping
Ji, Ming
Liu, Huijun
Liu, Chi
Qin, Xiaoqun
Xiang, Yang
author_sort Zhu, Jiahui
collection PubMed
description The mortality rate of idiopathic pulmonary fibrosis (IPF) increases yearly due to ineffective treatment. Given that the lung is exposed to the external environment, it is likely that oxidative stress, especially the stimulation of DNA, would be of particular importance in pulmonary fibrosis. DNA damage is known to play an important role in idiopathic pulmonary fibrosis initiation, so DNA repair systems targeting damage are also crucial for the survival of lung cells. Although many contemporary reports have summarized the role of individual DNA damage and repair pathways in their hypotheses, they have not focused on idiopathic pulmonary fibrosis. This review, therefore, aims to provide a concise overview for researchers to understand the pathways of DNA damage and repair and their roles in IPF.
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spelling pubmed-96871132022-11-25 The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis Zhu, Jiahui Liu, Lexin Ma, Xiaodi Cao, Xinyu Chen, Yu Qu, Xiangping Ji, Ming Liu, Huijun Liu, Chi Qin, Xiaoqun Xiang, Yang Antioxidants (Basel) Review The mortality rate of idiopathic pulmonary fibrosis (IPF) increases yearly due to ineffective treatment. Given that the lung is exposed to the external environment, it is likely that oxidative stress, especially the stimulation of DNA, would be of particular importance in pulmonary fibrosis. DNA damage is known to play an important role in idiopathic pulmonary fibrosis initiation, so DNA repair systems targeting damage are also crucial for the survival of lung cells. Although many contemporary reports have summarized the role of individual DNA damage and repair pathways in their hypotheses, they have not focused on idiopathic pulmonary fibrosis. This review, therefore, aims to provide a concise overview for researchers to understand the pathways of DNA damage and repair and their roles in IPF. MDPI 2022-11-19 /pmc/articles/PMC9687113/ /pubmed/36421478 http://dx.doi.org/10.3390/antiox11112292 Text en © 2022 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 Review
Zhu, Jiahui
Liu, Lexin
Ma, Xiaodi
Cao, Xinyu
Chen, Yu
Qu, Xiangping
Ji, Ming
Liu, Huijun
Liu, Chi
Qin, Xiaoqun
Xiang, Yang
The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title_full The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title_fullStr The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title_full_unstemmed The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title_short The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis
title_sort role of dna damage and repair in idiopathic pulmonary fibrosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687113/
https://www.ncbi.nlm.nih.gov/pubmed/36421478
http://dx.doi.org/10.3390/antiox11112292
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