Evidence map›Paper›PMID 24627571›Full record

ArticleAlcohol and alcoholism (Oxford, Oxfordshire)

Exogenous activation of Wnt/β-catenin signaling attenuates binge alcohol-induced deficient bone fracture healing.

Kristen L Lauing, Sumana Sundaramurthy, Rachel K Nauer, John J Callaci

Open access · bronzeAbstract read
In one paragraph

Article in Alcohol and alcoholism (Oxford, Oxfordshire). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Molecular pathogenesis of fracture nonunion.Journal of orthopaedic translation · 2018
    Review
  14. Development of controlled drug delivery systems for bone fracture-targeted therapeutic delivery: A review.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2018
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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

4 authors at 1 institution in 1 country.

Kristen L LauingAlcohol Research Program, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA Burn and Shock Trauma Institute, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA.
Sumana SundaramurthyAlcohol Research Program, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA Department of Orthopaedic Surgery and Rehabilitation, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA.
Rachel K NauerBurn and Shock Trauma Institute, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA.
John J CallaciAlcohol Research Program, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA Burn and Shock Trauma Institute, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA Department of Orthopaedic Surgery and Rehabilitation, Loyola University Stritch School of Medicine, 2160 S. 1st Ave, Maywood, IL 60546, USA jcallaci@lumc.edu.
Loyola University Chicago · US

Funding

Classifying Binge Alcohol-Induced Bone DamageR01AA016138 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI CALLACI, JOHN J. · 2006 to 2009
$987k
Alcohol Effects on SDF1-Mediated Stem Cell Homing Following Bone Fracture InjuryR21AA021225 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI CALLACI, JOHN J. · 2013 to 2014
$391k
NIAAA NIH HHS R01 AA016138NIAAA NIH HHS R21 AA021225PHS HHS F32 019613PHS HHS T32 013527
6 · The paper itself

Abstract

aimsExcessive alcohol consumption is associated with fracture non-union. Canonical Wnt pathway signaling activity regulates normal fracture healing. We previously demonstrated that binge alcohol exposure modulates β-catenin levels in the fracture callus of mice. Here, we sought to determine whether exogenous enhancement β-catenin signaling activity could restore normal fracture healing to binge-exposed mice.

methodsC57BL/6 male mice were exposed to episodic alcohol or saline for 6 total days of alcohol exposure over a 2-week period. Following alcohol exposure, mice were subjected to a stabilized mid-shaft tibia fracture. Beginning 4 days post-injury, mice received daily injections of either lithium chloride or saline subcutaneously. Protein levels of activated, inactivated, and total β-catenin and GSK-3β in fracture calluses were measured at post-injury day 9. Biomechanical strength testing and histology of callus tissue was assessed at post fracture day 14.

resultsBinge alcohol was associated with decreased callus biomechanical strength, and reduced cartilaginous callus formation. Alcohol decreased levels of callus-associated activated β-catenin while concomitantly increasing the levels of inactive β-catenin at post-injury day 9. Alcohol also increased callus associated activated GSK-3β at post-injury day 9. Lithium chloride (an inhibitor of GSK-3β) treatment increased activated β-catenin protein levels, significantly decreased activated GSK-3β and restored cartilaginous callus formation and endochondral ossification.

conclusionThese data link alcohol-impaired fracture healing with deregulation of Canonical Wnt signaling activity in the fracture callus. Exogenous activation of the Wnt pathway using LiCl attenuated the damaging effects of binge alcohol exposure on the fracture healing process by modulating canonical Wnt signaling activity.

Indexed as

Animalsbeta CateninBinge DrinkingBony CallusFracture HealingGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaLithium ChlorideMaleMiceSignal TransductionTibial FracturesWnt Signaling Pathwaybeta CateninGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseLithium Chloride

Identifiers

PMID24627571
PMCPMC4060733
OpenAlexW2036868006

What OpenQuestion holds

Textmetadata
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.