Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis

Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive...

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Autores principales: Lichun Qiao, Xuan Liu, Yujie He, Jiaheng Zhang, Hao Huang, Wenming Bian, Mumba Mulutula Chilufya, Yan Zhao, Jing Han
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/b0ff03a379664d329b9ada7a9ff3146c
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spelling oai:doaj.org-article:b0ff03a379664d329b9ada7a9ff3146c2021-11-11T17:21:21ZProgress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis10.3390/ijms2221119321422-00671661-6596https://doaj.org/article/b0ff03a379664d329b9ada7a9ff3146c2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11932https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in the environment and drinking water are major causes, and patients with skeletal fluorosis mainly present with symptoms of osteosclerosis, osteochondrosis, osteoporosis, and degenerative changes in joint cartilage. Etiologies for skeletal fluorosis have been established, but the specific pathogenesis is inconclusive. Currently, active osteogenesis and accelerated bone turnover are considered critical processes in the progression of skeletal fluorosis. In recent years, researchers have conducted extensive studies in fields of signaling pathways (Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hedgehog, parathyroid hormone, and insulin signaling pathways), stress pathways (oxidative stress and endoplasmic reticulum stress pathways), epigenetics (DNA methylation and non-coding RNAs), and their inter-regulation involved in the pathogenesis of skeletal fluorosis. In this review, we summarised and analyzed relevant findings to provide a basis for comprehensive understandings of the pathogenesis of skeletal fluorosis and hopefully propose more effective prevention and therapeutic strategies.Lichun QiaoXuan LiuYujie HeJiaheng ZhangHao HuangWenming BianMumba Mulutula ChilufyaYan ZhaoJing HanMDPI AGarticleskeletal fluorosisfluorideendemic diseasesignaling pathwaysepigeneticsendoplasmic reticulum stressBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11932, p 11932 (2021)
institution DOAJ
collection DOAJ
language EN
topic skeletal fluorosis
fluoride
endemic disease
signaling pathways
epigenetics
endoplasmic reticulum stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle skeletal fluorosis
fluoride
endemic disease
signaling pathways
epigenetics
endoplasmic reticulum stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
Lichun Qiao
Xuan Liu
Yujie He
Jiaheng Zhang
Hao Huang
Wenming Bian
Mumba Mulutula Chilufya
Yan Zhao
Jing Han
Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
description Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in the environment and drinking water are major causes, and patients with skeletal fluorosis mainly present with symptoms of osteosclerosis, osteochondrosis, osteoporosis, and degenerative changes in joint cartilage. Etiologies for skeletal fluorosis have been established, but the specific pathogenesis is inconclusive. Currently, active osteogenesis and accelerated bone turnover are considered critical processes in the progression of skeletal fluorosis. In recent years, researchers have conducted extensive studies in fields of signaling pathways (Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hedgehog, parathyroid hormone, and insulin signaling pathways), stress pathways (oxidative stress and endoplasmic reticulum stress pathways), epigenetics (DNA methylation and non-coding RNAs), and their inter-regulation involved in the pathogenesis of skeletal fluorosis. In this review, we summarised and analyzed relevant findings to provide a basis for comprehensive understandings of the pathogenesis of skeletal fluorosis and hopefully propose more effective prevention and therapeutic strategies.
format article
author Lichun Qiao
Xuan Liu
Yujie He
Jiaheng Zhang
Hao Huang
Wenming Bian
Mumba Mulutula Chilufya
Yan Zhao
Jing Han
author_facet Lichun Qiao
Xuan Liu
Yujie He
Jiaheng Zhang
Hao Huang
Wenming Bian
Mumba Mulutula Chilufya
Yan Zhao
Jing Han
author_sort Lichun Qiao
title Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
title_short Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
title_full Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
title_fullStr Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
title_full_unstemmed Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis
title_sort progress of signaling pathways, stress pathways and epigenetics in the pathogenesis of skeletal fluorosis
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/b0ff03a379664d329b9ada7a9ff3146c
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