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Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a severe progressive disease that may cause early right ventricular failure and eventual cardiac failure. The pathogenesis of PAH involves endothelial dysfunction, aberrant proliferation of pulmonary artery smooth muscle cells (PASMCs), and vascular fibrosis....

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Detalles Bibliográficos
Autores principales: Jiang, Yuan, Song, Shasha, Liu, Jingxin, Zhang, Liyuan, Guo, Xiaofei, Lu, Jiayao, Li, Lie, Yang, Chao, Fu, Qiang, Zeng, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518698/
https://www.ncbi.nlm.nih.gov/pubmed/37753070
http://dx.doi.org/10.3389/fimmu.2023.1206452
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author Jiang, Yuan
Song, Shasha
Liu, Jingxin
Zhang, Liyuan
Guo, Xiaofei
Lu, Jiayao
Li, Lie
Yang, Chao
Fu, Qiang
Zeng, Bin
author_facet Jiang, Yuan
Song, Shasha
Liu, Jingxin
Zhang, Liyuan
Guo, Xiaofei
Lu, Jiayao
Li, Lie
Yang, Chao
Fu, Qiang
Zeng, Bin
author_sort Jiang, Yuan
collection PubMed
description Pulmonary arterial hypertension (PAH) is a severe progressive disease that may cause early right ventricular failure and eventual cardiac failure. The pathogenesis of PAH involves endothelial dysfunction, aberrant proliferation of pulmonary artery smooth muscle cells (PASMCs), and vascular fibrosis. Hypoxia has been shown to induce elevated secretion of vascular endothelial growth factor (VEGF), leading to the development of hypoxic PAH. However, the molecular mechanisms underlying hypoxic PAH remain incompletely understood. Programmed cell death (PCD) is a natural cell death and regulated by certain genes. Emerging evidence suggests that apoptotic resistance contributes to the development of PAH. Moreover, several novel types of PCD, such as autophagy, pyroptosis, and ferroptosis, have been reported to be involved in the development of PAH. Additionally, multiple diverse epigenetic mechanisms including RNA methylation, DNA methylation, histone modification, and the non-coding RNA molecule-mediated processes have been strongly linked to the development of PAH. These epigenetic modifications affect the expression of genes, which produce important changes in cellular biological processes, including PCD. Consequently, a better understanding of the PCD processes and epigenetic modification involved in PAH will provide novel, specific therapeutic strategies for diagnosis and treatment. In this review, we aim to discuss recent advances in epigenetic mechanisms and elucidate the role of epigenetic modifications in regulating PCD in hypoxia-induced PAH.
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spelling pubmed-105186982023-09-26 Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension Jiang, Yuan Song, Shasha Liu, Jingxin Zhang, Liyuan Guo, Xiaofei Lu, Jiayao Li, Lie Yang, Chao Fu, Qiang Zeng, Bin Front Immunol Immunology Pulmonary arterial hypertension (PAH) is a severe progressive disease that may cause early right ventricular failure and eventual cardiac failure. The pathogenesis of PAH involves endothelial dysfunction, aberrant proliferation of pulmonary artery smooth muscle cells (PASMCs), and vascular fibrosis. Hypoxia has been shown to induce elevated secretion of vascular endothelial growth factor (VEGF), leading to the development of hypoxic PAH. However, the molecular mechanisms underlying hypoxic PAH remain incompletely understood. Programmed cell death (PCD) is a natural cell death and regulated by certain genes. Emerging evidence suggests that apoptotic resistance contributes to the development of PAH. Moreover, several novel types of PCD, such as autophagy, pyroptosis, and ferroptosis, have been reported to be involved in the development of PAH. Additionally, multiple diverse epigenetic mechanisms including RNA methylation, DNA methylation, histone modification, and the non-coding RNA molecule-mediated processes have been strongly linked to the development of PAH. These epigenetic modifications affect the expression of genes, which produce important changes in cellular biological processes, including PCD. Consequently, a better understanding of the PCD processes and epigenetic modification involved in PAH will provide novel, specific therapeutic strategies for diagnosis and treatment. In this review, we aim to discuss recent advances in epigenetic mechanisms and elucidate the role of epigenetic modifications in regulating PCD in hypoxia-induced PAH. Frontiers Media S.A. 2023-09-11 /pmc/articles/PMC10518698/ /pubmed/37753070 http://dx.doi.org/10.3389/fimmu.2023.1206452 Text en Copyright © 2023 Jiang, Song, Liu, Zhang, Guo, Lu, Li, Yang, Fu and Zeng https://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 Immunology
Jiang, Yuan
Song, Shasha
Liu, Jingxin
Zhang, Liyuan
Guo, Xiaofei
Lu, Jiayao
Li, Lie
Yang, Chao
Fu, Qiang
Zeng, Bin
Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title_full Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title_fullStr Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title_full_unstemmed Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title_short Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
title_sort epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518698/
https://www.ncbi.nlm.nih.gov/pubmed/37753070
http://dx.doi.org/10.3389/fimmu.2023.1206452
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