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活性氧簇驱动辐射诱导纤维化中的表观遗传改变。

Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.

机构信息

Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

出版信息

Oxid Med Cell Longev. 2019 Feb 6;2019:4278658. doi: 10.1155/2019/4278658. eCollection 2019.


DOI:10.1155/2019/4278658
PMID:30881591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6381575/
Abstract

Radiation-induced fibrosis (RIF) develops months to years after initial radiation exposure. RIF occurs when normal fibroblasts differentiate into myofibroblasts and lay down aberrant amounts of extracellular matrix proteins. One of the main drivers for developing RIF is reactive oxygen species (ROS) generated immediately after radiation exposure. Generation of ROS is known to induce epigenetic changes and cause differentiation of fibroblasts to myofibroblasts. Several antioxidant compounds have been shown to prevent radiation-induced epigenetic changes and the development of RIF. Therefore, reviewing the ROS-linked epigenetic changes in irradiated fibroblast cells is essential to understand the development and prevention of RIF.

摘要

辐射诱导纤维化(RIF)在初次辐射暴露数月至数年后发展。当正常成纤维细胞分化为肌成纤维细胞并沉积异常数量的细胞外基质蛋白时,就会发生 RIF。导致 RIF 发展的主要因素之一是辐射暴露后立即产生的活性氧(ROS)。众所周知,ROS 的产生会诱导表观遗传变化,并导致成纤维细胞向肌成纤维细胞分化。已经有几种抗氧化化合物被证明可以预防辐射诱导的表观遗传变化和 RIF 的发展。因此,回顾辐照成纤维细胞中与 ROS 相关的表观遗传变化对于理解 RIF 的发展和预防至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3006/6381575/2d48d8d6567b/OMCL2019-4278658.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3006/6381575/cf6258c07c05/OMCL2019-4278658.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3006/6381575/2d48d8d6567b/OMCL2019-4278658.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3006/6381575/cf6258c07c05/OMCL2019-4278658.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3006/6381575/2d48d8d6567b/OMCL2019-4278658.002.jpg

相似文献

[1]
Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.

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[7]
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[6]
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[7]
[A transcriptomic analysis of correlation between mitochondrial function and energy metabolism remodeling in mice with myocardial fibrosis following myocardial infarction].

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[8]
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[9]
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Redox Biol. 2024-4

[10]
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Sci Rep. 2024-1-2

本文引用的文献

[1]
The Protective Effect of New Compound XH-103 on Radiation-Induced GI Syndrome.

Oxid Med Cell Longev. 2018-7-4

[2]
α7‑nAchR agonist GTS‑21 reduces radiation‑induced lung injury.

Oncol Rep. 2018-8-1

[3]
LSD1 mediated changes in the local redox environment during the DNA damage response.

PLoS One. 2018-8-10

[4]
Antifibrotic Agent Pirfenidone Protects against Development of Radiation-Induced Pulmonary Fibrosis in a Murine Model.

Radiat Res. 2018-7-17

[5]
Taurine provides a time-dependent amelioration of the brain damage induced by γ-irradiation in rats.

J Hazard Mater. 2018-7-9

[6]
A Metabolomic Serum Signature from Nonhuman Primates Treated with a Radiation Countermeasure, Gamma-tocotrienol, and Exposed to Ionizing Radiation.

Health Phys. 2018-7

[7]
CpG-oligodeoxynucleotides may be effective for preventing ionizing radiation induced pulmonary fibrosis.

Toxicol Lett. 2018-4-19

[8]
hTERT peptide fragment GV1001 demonstrates radioprotective and antifibrotic effects through suppression of TGF‑β signaling.

Int J Mol Med. 2018-3-14

[9]
Post-Irradiation Treatment with a Superoxide Dismutase Mimic, MnTnHex-2-PyP, Mitigates Radiation Injury in the Lungs of Non-Human Primates after Whole-Thorax Exposure to Ionizing Radiation.

Antioxidants (Basel). 2018-3-7

[10]
Fractionated low-dose exposure to ionizing radiation leads to DNA damage, epigenetic dysregulation, and behavioral impairment.

Environ Epigenet. 2017-1-31

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