Evidence map›Paper›PMID 40533787›Full record

ArticleJournal of orthopaedic surgery and research2025

MiR-217 participates in the progression of postmenopausal osteoporosis by regulating the OPG/RANKL/RANK pathway.

Xiaoxia Yang, Qihua Jin, Lihua Guo

Abstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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.

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3 · Its place in the literature

Who cites it

44 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors.

Xiaoxia YangOncology Department, The First Affiliated Hospital of Nanjing University of Chinese Medicine, No.155, Hanzhong Road, Qinhuai District, Nanjing, 210023, China.
Qihua JinDepartment of Pulmonary Diseases, The First Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Lihua GuoOncology Department, The First Affiliated Hospital of Nanjing University of Chinese Medicine, No.155, Hanzhong Road, Qinhuai District, Nanjing, 210023, China. guolihua1189@163.com.

Funding

Yunnan Provincial Department of Science and Technology General Project 202301AZ070001-078
6 · The paper itself

Abstract

backgroundMicroRNAs regulate the OPG/RANKL/RANK signaling pathway, which is crucial for postmenopausal osteoporosis (PMO) development. Explore the role of miR-217 in PMO by regulating the OPG/RANKL/RANK signaling pathway.

methodsTaking osteoblast MC3T3-E1 as the research object, PMO model rats were further constructed. Reverse transcription quantitative PCR was used to detect the expression of miR-217 and related genes in cells and rat serum. Western blotting was used to detect the expression of relevant proteins. Enzyme-linked immunosorbent assay was used to detect the levels of related indicators in the serum of model rats.

resultsWith the osteogenic differentiation of MC3T3-E1 cells, the relative expression level of miR-217 gradually decreases. Overexpression of miR-217 inhibits cell proliferation and osteogenic differentiation, while promoting cell apoptosis. Conversely, the knockdown of miR-217 elicited opposite outcomes. miR-217 was demonstrated to target OPG and thereby influence MC3T3 - E1 cells, with potential involvement of the OPG/RANKL/RANK signaling pathway. Additionally, the expression of miR-217 in the serum of rats with the PMO model was upregulated. Conversely, the inhibition of miR-217 demonstrated the capacity to augment bone metabolism and osteogenic differentiation in these model rats. Additionally, miR-217 was found to specifically target OPG. Knockdown of miR-217 upregulates OPG, inhibits RANKL-RANK interaction, and suppresses the NF-κB/MAPK pathways.

conclusionsThe expression of miR-217 is upregulated in PMO, and it may participate in the progression of the disease by regulating the OPG/RANKL/RANK signaling pathway.

Indexed as

Disease ProgressionMicroRNAsOsteoporosis, PostmenopausalOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BSignal TransductionAnimalsCell DifferentiationCell LineCell ProliferationFemaleMiceOsteoblastsOsteogenesisRatsMicroRNAsOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BTnfrsf11b protein, ratMC3T3-E1 cellmiR-217OPG/RANKL/RANK pathwayPMO

Identifiers

PMID40533787
PMCPMC12175310

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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.