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SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic and debilitating disease that can exert serious and overwhelming effects on the physical and mental health of premature infants, predominantly due to intractable short- and long-term complications. Oxidative stress is one of the most predominant causes o...

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Detalles Bibliográficos
Autores principales: Yang, Kun, Dong, Wenbin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937618/
https://www.ncbi.nlm.nih.gov/pubmed/33693011
http://dx.doi.org/10.3389/fmed.2021.595634
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author Yang, Kun
Dong, Wenbin
author_facet Yang, Kun
Dong, Wenbin
author_sort Yang, Kun
collection PubMed
description Bronchopulmonary dysplasia (BPD) is a chronic and debilitating disease that can exert serious and overwhelming effects on the physical and mental health of premature infants, predominantly due to intractable short- and long-term complications. Oxidative stress is one of the most predominant causes of BPD. Hyperoxia activates a cascade of hazardous events, including mitochondrial dysfunction, uncontrolled inflammation, reduced autophagy, increased apoptosis, and the induction of fibrosis. These events may involve, to varying degrees, alterations in SIRT1 and its associated targets. In the present review, we describe SIRT1-related signaling pathways and their association with BPD. Our intention is to provide new insights into the molecular mechanisms that regulate BPD and identify potential therapeutic targets for this debilitating condition.
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spelling pubmed-79376182021-03-09 SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia Yang, Kun Dong, Wenbin Front Med (Lausanne) Medicine Bronchopulmonary dysplasia (BPD) is a chronic and debilitating disease that can exert serious and overwhelming effects on the physical and mental health of premature infants, predominantly due to intractable short- and long-term complications. Oxidative stress is one of the most predominant causes of BPD. Hyperoxia activates a cascade of hazardous events, including mitochondrial dysfunction, uncontrolled inflammation, reduced autophagy, increased apoptosis, and the induction of fibrosis. These events may involve, to varying degrees, alterations in SIRT1 and its associated targets. In the present review, we describe SIRT1-related signaling pathways and their association with BPD. Our intention is to provide new insights into the molecular mechanisms that regulate BPD and identify potential therapeutic targets for this debilitating condition. Frontiers Media S.A. 2021-02-22 /pmc/articles/PMC7937618/ /pubmed/33693011 http://dx.doi.org/10.3389/fmed.2021.595634 Text en Copyright © 2021 Yang and Dong. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Medicine
Yang, Kun
Dong, Wenbin
SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title_full SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title_fullStr SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title_full_unstemmed SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title_short SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
title_sort sirt1-related signaling pathways and their association with bronchopulmonary dysplasia
topic Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937618/
https://www.ncbi.nlm.nih.gov/pubmed/33693011
http://dx.doi.org/10.3389/fmed.2021.595634
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