Evidence map›Paper›PMID 34046950›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021

Vitamin D receptor activated by vitamin D administration alleviates Mycobacterium tuberculosis-induced bone destruction by inhibiting NFκB-mediated aberrant osteoclastogenesis.

Jiezhong Deng, Yusheng Yang, Jinyue He, Zhao Xie, Fei Luo, Jianzhong Xu, Zehua Zhang

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The potential role and value of vitamin D in the treatment of tuberculosis.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. The Research Progress in Immunotherapy of Tuberculosis.Frontiers in cellular and infection microbiology · 2021
    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

7 authors at 1 institution in 1 country.

Jiezhong DengDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0002-3637-7585
Yusheng YangDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jinyue HeDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Zhao XieDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Fei LuoDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jianzhong XuDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Zehua ZhangDepartment of Orthopedic Surgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinically, bone destruction caused by Mycobacterium tuberculosis was serious especially in patients with vitamin D (VD) deficiency. However, the role of VD in M. tuberculosis-induced bone destruction remains clear. In this context, we investigate the role of VD and vitamin D receptor (VDR) in the M. tuberculosis-induced bone destruction. First, we infected RAW264.7 and bone marrow-derived macrophages (BMMs) with Mycobacterium bovis Bacillus Calmette-Guérin (M. bovis BCG) in vitro. Then, we activated VDR through VD administration. TRAP and FAK staining, bone resorption assays, immunofluorescence staining, qPCR, and western blot were carried out. In vivo, the M. tuberculosis-induced osteolytic model on the murine skull was established and the μCT and histological analyses were performed. We found that VDR and TRAP were upregulated in bone tuberculosis tissue and proved that M. tuberculosis infection promoted osteoclastogenesis in RAW264.7 and BMMs. VD could inhibit osteoclasts differentiation, fusion, and bone resorption dose-dependently. However, when VDR was knocked down, the inhibitory effect of VD on osteoclasts disappeared. In mechanism, activation of VDR inhibits the phosphorylation of IκB α, thereby inhibiting NFκB signaling pathway and alleviating osteoclastogenesis. Furthermore, in the skull osteolysis model, VD administration reduced osteolysis, but not in VDR

Indexed as

AnimalsMacrophagesMaleMiceMice, Inbred C57BLMycobacterium tuberculosisNF-kappa BOsteolysisReceptors, CalcitriolTuberculosisVitamin DVitaminsNF-kappa BReceptors, CalcitriolVitamin DVitaminsMycobacterium tuberculosisosteoclastogenesisVDRvitamin D

Identifiers

PMID34046950
PMCPMC12315972
OpenAlexW3165220115

What OpenQuestion holds

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LicenceCC BY-NC
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.