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

Qiao, Lichun, Liu, Xuan, He, Yujie, Zhang, Jiaheng, Huang, Hao, Bian, Wenming, Chilufya, Mumba Mulutula, Zhao, Yan, Han, Jing·2021·International Journal of Molecular Sciences
DOI 10.3390/ijms222111932PMC PMC8584317
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Abstract

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.

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Figure 1 Wnt/β-catenin signaling pathway in the pathogenesis of skeletal fluorosis. (a) Wnt signaling is inhibited; (b) Wnt signaling is activated. GSK-3β: glycogen synthase kinase-3β; Dkk-1: dickkopf-related protein 1; LRP5/6: low-density lipoprotein receptor-related protein 5/6; TCF/LEF: T-cell factor/lymphatic enhancer factor; Runx2: Runt-related transcription factor 2; SOST: serum sclerostin.
Figure 1 Wnt/β-catenin signaling pathway in the pathogenesis of skeletal fluorosis. (a) Wnt signaling is inhibited; (b) Wnt signaling is activated. GSK-3β: glycogen synthase kinase-3β; Dkk-1: dickkopf-related protein 1; LRP5/6: low-density lipoprotein receptor-related protein 5/6; TCF/LEF: T-cell factor/lymphatic enhancer factor; Runx2: Runt-related transcription factor 2; SOST: serum sclerostin.CC BY · PubMed Central
Figure 2 Notch signaling pathway in the pathogenesis of skeletal fluorosis. NICD: Notch intracellular structural domain; RBP-J: Recombination signal binding protein-Jκ; CSL: Epstein-Barr virus latency C promoter binding factor 1/repressor of hairless/Lag1.
Figure 2 Notch signaling pathway in the pathogenesis of skeletal fluorosis. NICD: Notch intracellular structural domain; RBP-J: Recombination signal binding protein-Jκ; CSL: Epstein-Barr virus latency C promoter binding factor 1/repressor of hairless/Lag1.CC BY · PubMed Central
Figure 3 PI3K/Akt/mTOR signaling pathway in the pathogenesis of skeletal fluorosis. S6K1: ribosomal protein S6 kinase β-1; 4EBP1: 4E binding protein 1; LC3: light chain 3; TSC1/2: tuberous sclerosis protein complex1/2.
Figure 3 PI3K/Akt/mTOR signaling pathway in the pathogenesis of skeletal fluorosis. S6K1: ribosomal protein S6 kinase β-1; 4EBP1: 4E binding protein 1; LC3: light chain 3; TSC1/2: tuberous sclerosis protein complex1/2.CC BY · PubMed Central
Figure 4 Hedgehog signaling pathway in the pathogenesis of skeletal fluorosis. Ptch: Ptched; Smo: Smoothened; Ihh: Indian Hedgehog; Shh: Sonic Hedgehog; Gli1 and Gli2: 5-zinc finger transcription factor Glis; Bcl-2: B cell lymphoma /leukemia-2; BMP-2: bone morphogenetic protein-2; Bax: B cell lymphoma/leukemia gene associated x.
Figure 4 Hedgehog signaling pathway in the pathogenesis of skeletal fluorosis. Ptch: Ptched; Smo: Smoothened; Ihh: Indian Hedgehog; Shh: Sonic Hedgehog; Gli1 and Gli2: 5-zinc finger transcription factor Glis; Bcl-2: B cell lymphoma /leukemia-2; BMP-2: bone morphogenetic protein-2; Bax: B cell lymphoma/leukemia gene associated x.CC BY · PubMed Central
Figure 5 PTH signaling pathway in the pathogenesis of skeletal fluorosis. PTH: parathyroid hormone; PTH1R: parathyroid hormone receptor; RANKL: receptor activator of nuclear factor-κB ligand.
Figure 5 PTH signaling pathway in the pathogenesis of skeletal fluorosis. PTH: parathyroid hormone; PTH1R: parathyroid hormone receptor; RANKL: receptor activator of nuclear factor-κB ligand.CC BY · PubMed Central
Figure 6 Interactive regulatory networks among Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hh, PTH, and insulin signaling pathways involved in skeletal fluorosis.
Figure 6 Interactive regulatory networks among Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hh, PTH, and insulin signaling pathways involved in skeletal fluorosis.CC BY · PubMed Central

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Metadata

Authors
Qiao, L., Liu, X., He, Y., Zhang, J., Huang, H., Bian, W., Chilufya, M. M., Zhao, Y., & Han, J.
Affiliations
Key Laboratory of Environment and Genes Related to Diseases, School of Public Health, Health Science Center, Xi’an Jiaotong University, Xi’an 710049, China
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2021-11-03
Volume
22
Issue
21
Pages
11932
ISSN
1422-0067
DOI
10.3390/ijms222111932
PMC
PMC8584317
Cited by
64
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Natural Science Foundation of China (81872567)
  • Shaanxi Province Key Research and Development (2018ZDCXL-SF-02-03-01)

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