Evidence map›Paper›PMID 31025251›Full record

ArticleIn vitro cellular & developmental biology. Animal2019

miR-363-3p is activated by MYB and regulates osteoporosis pathogenesis via PTEN/PI3K/AKT signaling pathway.

Mingyi Li, Ruolan Luo, Wenjian Yang, Zhen Zhou, Chenxia Li

Abstract read
PubMed Publisher
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  7. Common miRNAs of Osteoporosis and Fibromyalgia: A Review.International journal of molecular sciences · 2023
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  12. Regulation of osteoclast-mediated bone resorption by microRNA.Cellular and molecular life sciences : CMLS · 2022
    Review
  13. Bone Regeneration and Oxidative Stress: An Updated Overview.Antioxidants (Basel, Switzerland) · 2022
    Review
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  17. Total flavonoids ofExperimental and therapeutic medicine · 2021
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  18. Review
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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

5 authors at 2 institutions in 1 country.

Mingyi LiEndocrine Department, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, Hubei, China.ORCID http://orcid.org/0000-0002-4916-7456
Ruolan LuoEndocrine Department, Xiangyang Hospital of Traditional Chinese Medicine, No.24, Changzheng Road, Xiangyang, 441000, Hubei, China. Ruolan_Luo@163.com.
Wenjian YangEndocrine Department, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, Hubei, China.
Zhen ZhouEndocrine Department, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, Hubei, China.
Chenxia LiEndocrine Department, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, Hubei, China.
Hubei University of Medicine · CNXiangyang Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis results from the imbalance between osteogenesis and bone resorption mediated by osteoblasts and osteoclasts. During the disease process of osteoporosis, the alteration of gene expression occurs, which lead to the disease progression. MicroRNAs (miRNAs) have been previously demonstrated to be modulators for bone metabolism via regulation of osteoblast and osteoclast differentiation. In the present study, we detected the expression levels of five osteoporosis-related miRNAs in bone and serum samples of patient with or without osteoporosis. The downstream molecular mechanism of miR-363-3p was analyzed and detected by using bioinformatics analysis and mechanism experiment. The upstream transcription factor of miR-363-3p was analyzed by applying bioinformatics analysis and ChIP assay and luciferase reporter assay. The role of this pathway in osteoclastogenesis was demonstrated by functional assays. MiR-363-3p was significantly highly expressed in osteoporotic samples. Mechanistically, miR-363-3p promotes osteoclastogenesis and inhibits osteogenic differentiation by targeting PTEN and therefore activating PI3K/AKT signaling pathway. MiR-363-3p was activated by its upstream transcription activator MYB. This study revealed that MYB-induced upregulation of miR-363-3p regulates osteoporosis pathogenesis via PTEN/PI3K/AKT signaling pathway.

Indexed as

Bone and BonesBone ResorptionCell DifferentiationComputational BiologyGene Expression RegulationHumansMicroRNAsOsteoblastsOsteoclastsOsteogenesisOsteoporosisPatientsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mybPTEN PhosphohydrolaseMicroRNAsMIRN363 microRNA, humanMYB protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mybPTEN PhosphohydrolasePTEN protein, humanmiR-363-3pMYBOsteoporosisPI3K/AKT signaling pathwayPTEN

Identifiers

PMID31025251
OpenAlexW2941231533

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.