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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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) |
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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 |
work_keys_str_mv |
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