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Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension

Pulmonary hypertension (PH) is a severe progressive lung disorder characterized by pulmonary vasoconstriction and vascular remodeling, culminating in right-sided heart failure and increased mortality. Data from animal models and human subjects demonstrated that hypoxia-inducible factor (HIF)-related...

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Autores principales: Zeidan, Esraa M., Hossain, Mohammad Akbar, El-Daly, Mahmoud, Abourehab, Mohammed A. S., Khalifa, Mohamed M. A., Taye, Ashraf
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9457092/
https://www.ncbi.nlm.nih.gov/pubmed/36079149
http://dx.doi.org/10.3390/jcm11175219
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author Zeidan, Esraa M.
Hossain, Mohammad Akbar
El-Daly, Mahmoud
Abourehab, Mohammed A. S.
Khalifa, Mohamed M. A.
Taye, Ashraf
author_facet Zeidan, Esraa M.
Hossain, Mohammad Akbar
El-Daly, Mahmoud
Abourehab, Mohammed A. S.
Khalifa, Mohamed M. A.
Taye, Ashraf
author_sort Zeidan, Esraa M.
collection PubMed
description Pulmonary hypertension (PH) is a severe progressive lung disorder characterized by pulmonary vasoconstriction and vascular remodeling, culminating in right-sided heart failure and increased mortality. Data from animal models and human subjects demonstrated that hypoxia-inducible factor (HIF)-related signaling is essential in the progression of PH. This review summarizes the regulatory pathways and mechanisms of HIF-mediated signaling, emphasizing the role of mitochondria in HIF regulation and PH pathogenesis. We also try to determine the potential to therapeutically target the components of the HIF system for the management of PH.
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spelling pubmed-94570922022-09-09 Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension Zeidan, Esraa M. Hossain, Mohammad Akbar El-Daly, Mahmoud Abourehab, Mohammed A. S. Khalifa, Mohamed M. A. Taye, Ashraf J Clin Med Review Pulmonary hypertension (PH) is a severe progressive lung disorder characterized by pulmonary vasoconstriction and vascular remodeling, culminating in right-sided heart failure and increased mortality. Data from animal models and human subjects demonstrated that hypoxia-inducible factor (HIF)-related signaling is essential in the progression of PH. This review summarizes the regulatory pathways and mechanisms of HIF-mediated signaling, emphasizing the role of mitochondria in HIF regulation and PH pathogenesis. We also try to determine the potential to therapeutically target the components of the HIF system for the management of PH. MDPI 2022-09-03 /pmc/articles/PMC9457092/ /pubmed/36079149 http://dx.doi.org/10.3390/jcm11175219 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
Zeidan, Esraa M.
Hossain, Mohammad Akbar
El-Daly, Mahmoud
Abourehab, Mohammed A. S.
Khalifa, Mohamed M. A.
Taye, Ashraf
Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title_full Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title_fullStr Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title_full_unstemmed Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title_short Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
title_sort mitochondrial regulation of the hypoxia-inducible factor in the development of pulmonary hypertension
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9457092/
https://www.ncbi.nlm.nih.gov/pubmed/36079149
http://dx.doi.org/10.3390/jcm11175219
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