Evidence map›Paper›PMID 36797542›Full record

ArticleExperimental & molecular medicine2023

Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing.

Shi-Dan Li, Wei Xing, Shao-Chuan Wang, You-Bin Li, Hao Jiang, Han-Xuan Zheng, Xiao-Ming Li, Jing Yang, De-Bin Guo, Xiao-Yu Xie and 5 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Lung Inflammatory Phenotype in Mice Deficient in Fibulin-2 and ADAMTS-12.International journal of molecular sciences · 2024
    Article
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

15 authors at 4 institutions in 2 countries.

Shi-Dan LiDepartment of Orthopaedics, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Wei XingDepartment of Stem Cell and Regenerative Medicine, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Shao-Chuan WangDepartment of Orthopaedics, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
You-Bin LiDepartment of Orthopaedics, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Hao JiangDepartment of Orthopaedics, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, People's Republic of China.
Han-Xuan ZhengDepartment of Nursing, Montreal Neurological Hospital, 3801 Rue University, Montréal, QC H3A 2B4, Canada.
Xiao-Ming LiDepartment of Military Traffic Injury Prevention, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Jing YangDepartment of Emergency, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
De-Bin GuoDepartment of Emergency, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Xiao-Yu XieDepartment of Orthopaedics, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Ren-Qing JiangDepartment for Combat Casualty Care Training, Training Base for Army Health Care, Third Military Medical University, Chongqing, 400042, People's Republic of China.
Chao FanMedical Research Center, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University, Southwest Jiaotong University, Chengdu, 610031, People's Republic of China.
Lei LiDepartment of Stem Cell and Regenerative Medicine, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Xiang XuDepartment of Stem Cell and Regenerative Medicine, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China. xiangxu@tmmu.edu.cn.ORCID 0000-0002-1026-2210
Jun FeiDepartment of Emergency, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China. feijundoctor@sohu.com.
Army Medical University · CNAffiliated Hospital of Southwest Medical University · CNMontreal Neurological Institute and Hospital · CASouthwest Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone fracture remains a common occurrence, with a population-weighted incidence of approximately 3.21 per 1000. In addition, approximately 2% to 50% of patients with skeletal fractures will develop an infection, one of the causes of disordered bone healing. Dysfunction of bone marrow mesenchymal stem cells (BMSCs) plays a key role in disordered bone repair. However, the specific mechanisms underlying BMSC dysfunction caused by bone infection are largely unknown. In this study, we discovered that Fibulin2 expression was upregulated in infected bone tissues and that BMSCs were the source of infection-induced Fibulin2. Importantly, Fibulin2 knockout accelerated mineralized bone formation during skeletal development and inhibited inflammatory bone resorption. We demonstrated that Fibulin2 suppressed BMSC osteogenic differentiation by binding to Notch2 and inactivating the Notch2 signaling pathway. Moreover, Fibulin2 knockdown restored Notch2 pathway activation and promoted BMSC osteogenesis; these outcomes were abolished by DAPT, a Notch inhibitor. Furthermore, transplanted Fibulin2 knockdown BMSCs displayed better bone repair potential in vivo. Altogether, Fibulin2 is a negative regulator of BMSC osteogenic differentiation that inhibits osteogenesis by inactivating the Notch2 signaling pathway in infected bone.

Indexed as

Fracture HealingOsteogenesisBone and BonesBone Marrow CellsCalcium-Binding ProteinsCell DifferentiationCells, CulturedExtracellular Matrix ProteinsHumansSignal TransductionStem CellsCalcium-Binding ProteinsExtracellular Matrix Proteinsfibulin 2

Identifiers

PMID36797542
PMCPMC9981700
OpenAlexW4321164842

What OpenQuestion holds

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LicenceCC BY
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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.