Evidence map›Paper›PMID 39106008›Full record

ArticleBiological trace element research2025

Knockdown of SMYD3 by RNA Interference Regulates the Expression of Autophagy-Related Proteins and Inhibits Bone Formation in Fluoride-Exposed Osteoblasts.

Jie Deng, Xiaoxiao Zeng, Kailin Zhang, Ting Zhang, Yangting Dong, Jian Zou, Changxue Wu, Yi Li, Fucheng Li, Zhizhong Guan

Abstract read
In one paragraph

Article in Biological trace element research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Jie DengKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Xiaoxiao ZengKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Kailin ZhangKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Ting ZhangKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Yangting DongKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Jian ZouKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Changxue WuKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Yi LiKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.
Fucheng LiResearch Group of Liupanshui Center for Disease Control and Prevention, Liupanshui, 553001, Guizhou, China.
Zhizhong GuanKey Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China. zzg@gmc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to explore the role of histone methyltransferase SET and MYND domain containing 3 (SMYD3) in bone metabolism of osteoblasts exposed to fluoride. The levels of urine fluoride, BALP, and OC and the mRNA expression of SMYD3 were determined in patients with skeletal fluorosis and non-fluoride-exposed people on informed consent. The expression of SMYD3 protein, OC contents, and BALP activities were detected in human osteoblast-like MG63 cells and rat primary osteoblasts treated with sodium fluoride (NaF) for 48 h. The autophagosomes were observed by transmission electron microscopy. Then, we knocked down SMYD3 to confirm whether it was involved in the regulation of bone formation and related to autophagy and Wnt/β-catenin pathway. We observed that OC and BALP levels in patients with skeletal fluorosis significantly increased, while the mRNA expression of SMYD3 significantly decreased in the skeletal fluorosis groups. In vitro, the OC contents, BALP activities, and expression of SMYD3 significantly increased, and many autophagosomes were observed in NaF treated osteoblasts. The downregulation of SMYD3 significantly inhibited OC contents, BALP activities, and expression of autophagy-related proteins, but with no significant changes in the Wnt/β-catenin pathway. Our results demonstrated that fluoride exposure with coal-burning pollution caused orthopedic injuries and abnormalities in the levels of OC and BALP and hindered normal bone metabolism. Silencing the SMYD3 gene could significantly reduce OC and BALP levels via inhibiting the increase in autophagy induced by fluoride.

Indexed as

AutophagyFluoridesHistone-Lysine N-MethyltransferaseOsteoblastsOsteogenesisRNA InterferenceAdultAnimalsFemaleGene Knockdown TechniquesHumansMaleRatsSodium FluorideFluoridesHistone-Lysine N-MethyltransferaseSMYD3 protein, humanSodium FluorideAlkaline phosphataseAutophagyOsteoblastOsteocalcinSET and MYND domain containing 3Wnt/β-catenin pathway

Identifiers

PMID39106008
PMCPMC11919934

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.