Evidence map›Paper›PMID 36434613›Full record

ArticleBMC musculoskeletal disorders2022

Nuclear factor erythroid 2-related factor 2 (Nrf2) deficiency causes age-dependent progression of female osteoporosis.

Yusuke Kubo, Jesus Abraham Herrera Gonzalez, Rainer Beckmann, Marek Weiler, Helda Pahlavani, Mauricio Cruz Saldivar, Katharina Szymanski, Stefanie Rosenhain, Athanassios Fragoulis, Sander Leeflang and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC musculoskeletal disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
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

19 authors at 3 institutions in 2 countries.

Yusuke KuboDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany. ykubo@ukaachen.de.
Jesus Abraham Herrera GonzalezDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Rainer BeckmannDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Marek WeilerInstitute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.
Helda PahlavaniDepartment of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.
Mauricio Cruz SaldivarDepartment of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.
Katharina SzymanskiDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Stefanie RosenhainInstitute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.
Athanassios FragoulisDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Sander LeeflangDepartment of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.
Alexander SlowikDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Felix GremseInstitute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.
Michael WolfDepartment of Orthodontics, Uniklinik RWTH Aachen, Pauwelsstraße 30, 52074, Aachen, Germany.
Mohammad Javad MirzaaliDepartment of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.
Amir Abbas ZadpoorDepartment of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.
Christoph Jan WruckDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Thomas PufeDepartment of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Mersedeh Tohidnezhad *Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Holger Jahr *Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
RWTH Aachen University · DEUniversitätsklinikum Aachen · DEDelft University of Technology · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor for cellular redox homeostasis. The association of Nrf2 with elderly female osteoporotic has yet to be fully described. The aim was to elucidate a potential age-dependent Nrf2 contribution to female osteoporosis in mice.

methodsEighteen female wild type (WT) and 16 Nrf2-knockout (KO) mice were sacrificed at different ages (12 weeks = young mature adult and 90 weeks = old) to analyze their femurs. The morphological properties (trabecular and cortical) were evaluated by micro-computed tomography (μCT) and compared to gold standard histochemistry analysis. The quasi-static compression tests were performed to calculate the mechanical properties of bones. Additionally, the population of bone resorbing cells and aromatase expression by osteocytes was immunohistochemically evaluated and empty osteocyte lacunae was counted in cortical bone.

resultsOld Nrf2-KO mice revealed a significantly reduced trabecular bone mineral density (BMD), cortical thickness, cortical area, and bone fraction compared to old WT mice, regardless of no significant difference in skeletally mature young adult mice between WT and KO. Specifically, while all old WT mice showed thin metaphyseal trabeculae, trabecular bone was completely absent in 60% of old KO mice. Additionally, old KO mice showed significantly more osteoclast-like cells and fewer aromatase-positive osteocytes than WT mice, whereas the occurrence of empty osteocyte lacunae did not differ between both groups. Nrf2-KO mice further showed an age-dependently reduced fracture resilience compared to age-matched WT mice.

conclusionOur results suggest that chronic Nrf2 loss can lead to age-dependent progression of female osteoporosis.

Indexed as

NF-E2-Related Factor 2OsteoporosisAnimalsAromataseFemaleMiceMice, Inbred C57BLMice, KnockoutX-Ray MicrotomographyAromataseNF-E2-Related Factor 2Bone strengthEstrogenFracture resilienceNrf2Osteoporosis

Identifiers

PMID36434613
PMCPMC9700883
OpenAlexW4310054431

What OpenQuestion holds

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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.