Evidence map›Paper›PMID 29497762›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2018

Pharmacological inhibition of IL-6 trans-signaling improves compromised fracture healing after severe trauma.

Kathrin Kaiser, Katja Prystaz, Anna Vikman, Melanie Haffner-Luntzer, Stephanie Bergdolt, Gudrun Strauss, Georg H Waetzig, Stefan Rose-John, Anita Ignatius

Open access · hybridAbstract read
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  8. Physiologic impact of inflammation in the polytrauma patient.OTA international : the open access journal of orthopaedic trauma · 2025
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  17. Selective inhibition of interleukin 6 receptor decreased inflammatory cytokines and increased proteases in an experimental model of critical calvarial defect.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
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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

9 authors at 3 institutions in 1 country.

Kathrin KaiserInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany.
Katja PrystazInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany.
Anna VikmanInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany.
Melanie Haffner-LuntzerInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany.
Stephanie BergdoltInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany.
Gudrun StraussDepartment of Pediatrics and Adolescent Medicine, University Medical Center Ulm, 89075, Ulm, Germany.
Georg H WaetzigCONARIS Research Institute AG, 24118, Kiel, Germany.
Stefan Rose-JohnInstitute of Biochemistry, Christian-Albrechts-University of Kiel, 24118, Kiel, Germany.
Anita IgnatiusInstitute of Orthopedic Research and Biomechanics, Trauma Research Center Ulm, University Medical Center Ulm, 89081, Ulm, Germany. anita.ignatius@uni-ulm.de.ORCID 0000-0002-4782-1979
Christian-Albrechts-Universität zu Kiel · DEConaris · DEUniversität Ulm · DE

Funding

Deutsche Forschungsgemeinschaft INST40/491-1Deutsche Forschungsgemeinschaft (DE) CRC841, CRC877
6 · The paper itself

Abstract

Patients with multiple injuries frequently suffer bone fractures and are at high risk to develop fracture healing complications. Because of its key role both in systemic posttraumatic inflammation and fracture healing, the pleiotropic cytokine interleukin-6 (IL-6) may be involved in the pathomechanisms of trauma-induced compromised fracture healing. IL-6 signals are transmitted by two different mechanisms: classic signaling via the membrane-bound receptor (mIL-6R) and trans-signaling via its soluble form (sIL-6R). Herein, we investigated whether IL-6 classic and trans-signaling play different roles in bone regeneration after severe injury. Twelve-week-old C57BL/6J mice underwent combined femur osteotomy and thoracic trauma. To study the function of IL-6, either an anti-IL-6 antibody, which inhibits both IL-6 classic and trans-signaling, or a soluble glycoprotein 130 fusion protein (sgp130Fc), which selectively blocks trans-signaling, were injected 30 min and 48 h after surgery. Bone healing was assessed using cytokine analyses, flow cytometry, histology, micro-computed tomography, and biomechanical testing. Selective inhibition of IL-6 trans-signaling significantly improved the fracture healing outcome after combined injury, as confirmed by accelerated cartilage-to-bone transformation, enhanced bony bridging of the fracture gap and improved mechanical callus properties. In contrast, global IL-6 inhibition did not affect compromised fracture healing. These data suggest that classic signaling may mediate beneficial effects on bone repair after severe injury. Selective inhibition of IL-6 trans-signaling might have therapeutic potential to treat fracture healing complications in patients with concomitant injuries.

Indexed as

AnimalsAntibodiesCytokinesFemurFracture HealingMaleMice, Inbred C57BLOsteotomyRecombinant Fusion ProteinsSignal TransductionThoracic InjuriesWounds and InjuriesX-Ray MicrotomographyAntibodiesCytokinesolamkiceptRecombinant Fusion ProteinsBone fracture healingClassic signalingIL-6InflammationTrans-signalingTrauma

Identifiers

PMID29497762
PMCPMC5889421
OpenAlexW2789334209

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.