Evidence map›Paper›PMID 35216216›Full record

ArticleInternational journal of molecular sciences2022

Effect of Oxidative Stress-Induced Apoptosis on Active FGF23 Levels in MLO-Y4 Cells: The Protective Role of 17-β-Estradiol.

Vladana Domazetovic, Irene Falsetti, Simone Ciuffi, Teresa Iantomasi, Gemma Marcucci, Maria Teresa Vincenzini, Maria Luisa Brandi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Nrf2 signaling pathway: focus on oxidative stress in osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Review
  4. Article
  5. Article
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  9. 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

7 authors at 1 institution in 1 country.

Vladana DomazetovicDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.ORCID 0000-0001-8307-5662
Irene FalsettiDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Simone CiuffiDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.ORCID 0000-0002-1788-4426
Teresa IantomasiDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.ORCID 0000-0001-7461-330X
Gemma MarcucciDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Maria Teresa VincenziniDepartment of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy.
Maria Luisa BrandiFondazione Italiana Ricerca sulle Malattie dell'Osso (FIRMO Onlus), 50141 Florence, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery that osteocytes secrete phosphaturic fibroblast growth factor 23 (FGF23) has defined bone as an endocrine organ. However, the autocrine and paracrine functions of FGF23 are still unknown. The present study focuses on the cellular and molecular mechanisms involved in the complex control of FGF23 production and local bone remodeling functions. FGF23 was assayed using ELISA kit in the presence or absence of 17β-estradiol in starved MLO-Y4 osteocytes. In these cells, a relationship between oxidative stress-induced apoptosis and up-regulation of active FGF23 levels due to MAP Kinases activation with involvement of the transcriptional factor (NF-kB) has been demonstrated. The active FGF23 increase can be due to up-regulation of its expression and post-transcriptional modifications. 17β-estradiol prevents the increase of FGF23 by inhibiting JNK and NF-kB activation, osteocyte apoptosis and by the down-regulation of osteoclastogenic factors, such as sclerostin. No alteration in the levels of dentin matrix protein 1, a FGF23 negative regulator, has been determined. The results of this study identify biological targets on which drugs and estrogen may act to control active FGF23 levels in oxidative stress-related bone and non-bone inflammatory diseases.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisBone and BonesBone RemodelingCell LineDown-RegulationEstradiolEstrogensFibroblast Growth Factor-23Gene Expression RegulationMiceOsteocytesOsteogenesisOxidative StressProtective AgentsAdaptor Proteins, Signal TransducingEstradiolEstrogensFgf23 protein, mouseFibroblast Growth Factor-23Protective AgentsestrogenFGF23oxidative stress-induced apoptosis

Identifiers

PMID35216216
PMCPMC8879671
OpenAlexW4213054682

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.