Evidence map›Paper›PMID 27410432›Full record

ArticlePloS one2016

Inhibition of Midkine Augments Osteoporotic Fracture Healing.

Melanie Haffner-Luntzer, Julia Kemmler, Verena Heidler, Katja Prystaz, Thorsten Schinke, Michael Amling, Anna Kovtun, Anna E Rapp, Anita Ignatius, Astrid Liedert

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
1.3field-weighted citation impact, top 21% 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, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

10 authors at 2 institutions in 1 country.

Melanie Haffner-LuntzerInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Julia KemmlerInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Verena HeidlerInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Katja PrystazInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Thorsten SchinkeInstitute of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michael AmlingInstitute of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anna KovtunInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Anna E RappInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Anita IgnatiusInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Astrid LiedertInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heparin-binding growth and differentiation factor midkine (Mdk) is proposed to negatively regulate osteoblast activity and bone formation in the adult skeleton. As Mdk-deficient mice were protected from ovariectomy (OVX)-induced bone loss, this factor may also play a role in the pathogenesis of postmenopausal osteoporosis. We have previously demonstrated that Mdk negatively influences bone regeneration during fracture healing. Here, we investigated whether the inhibition of Mdk using an Mdk-antibody (Mdk-Ab) improves compromised bone healing in osteoporotic OVX-mice. Using a standardized femur osteotomy model, we demonstrated that Mdk serum levels were significantly enhanced after fracture in both non-OVX and OVX-mice, however, the increase was considerably greater in osteoporotic mice. Systemic treatment with the Mdk-Ab significantly improved bone healing in osteoporotic mice by increasing bone formation in the fracture callus. On the molecular level, we demonstrated that the OVX-induced reduction of the osteoanabolic beta-catenin signaling in the bony callus was abolished by Mdk-Ab treatment. Furthermore, the injection of the Mdk-Ab increased trabecular bone mass in the skeleton of the osteoporotic mice. These results implicate that antagonizing Mdk may be useful for the therapy of osteoporosis and osteoporotic fracture-healing complications.

Indexed as

AnimalsAntibodiesbeta CateninBone RegenerationBony CallusCancellous BoneCytokinesFemaleMiceMice, Inbred C57BLMidkineOsteogenesisOsteoporosisOsteoporotic FracturesAntibodiesbeta CateninCytokinesMidkine

Identifiers

PMID27410432
PMCPMC4943649
OpenAlexW2468963407

What OpenQuestion holds

Textmetadata
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.