Evidence map›Paper›PMID 26963322›Full record

ArticleCritical care medicine2016

Inhibition of Plexin C1 Protects Against Hepatic Ischemia-Reperfusion Injury.

Klemens König, Tiago Granja, Veit-Simon Eckle, Valbona Mirakaj, David Köhler, Martin Schlegel, Peter Rosenberger

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Article in Critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. Hypoxia-inducible factor-dependent induction of myeloid-derived netrin-1 attenuates natural killer cell infiltration during endotoxin-induced lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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  7. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Klemens König1Department of Anaesthesiology and Intensive Care Medicine, Tübingen University Hospital, Eberhard-Karls University Tübingen, Tübingen, Germany. 2Clinic of Anaesthesiology, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt am Main, Johann Wolfgang Goethe University, Tübingen, Germany.
Tiago Granja
Veit-Simon Eckle
Valbona Mirakaj
David Köhler
Martin Schlegel
Peter Rosenberger
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesHepatic ischemia-reperfusion injury is a disease pattern that is associated with an acute inflammatory reaction. It is well known that neutrophils play an essential role in the early phase of hepatic ischemia-reperfusion injury and determine the extent of tissue damage. Hepatic ischemia-reperfusion injury can result in organ failure, which is linked to high mortality. Recent data indicate that the neuronal guidance receptor Plexin C1 is involved in the control of the acute inflammatory response and, as such, modulates the transmigration of neutrophils. Hence, we investigated the functional role of Plexin C1 in a mouse model of early hepatic ischemia-reperfusion injury.

designAnimal study.

settingUniversity experimental laboratory. SUBJECTS: Wild-type, PLXNC1 and chimeric mice.

interventionsHepatic ischemia-reperfusion injury or sham operation. MEASUREMENTS AND MAIN

resultsWe found that the functional inhibition of Plexin C1 in wild-type mice treated with an anti-Plexin C1 antibody and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the levels of lactate dehydrogenase, aspartate, and alanine aminotransferase. This reduction in ischemia-reperfusion injury was accompanied by reduced numbers of neutrophils in ischemic hepatic tissue and reduced serum levels of inflammatory cytokines. Experiments using Plexin C1 receptor-deficient (PLXNC1) mice also demonstrated decreased hepatic ischemia-reperfusion injury. Studies of chimeric mice revealed that the hematopoietic Plexin C1 knockout is crucial for reducing the extent of hepatic ischemia-reperfusion injury.

conclusionsThese results describe a role for Plexin C1 during ischemia-reperfusion injury, highlight the role of hematopoietic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Plexin C1 is a potential drug target.

Indexed as

Alanine TransaminaseAnimalsAntigens, CDAspartic AcidCell Adhesion Molecules, NeuronalDisease Models, AnimalGPI-Linked ProteinsInflammation MediatorsLiverL-Lactate DehydrogenaseMaleMiceNeutrophilsReperfusion InjurySemaphorinsAlanine TransaminaseAntigens, CDAspartic AcidCell Adhesion Molecules, NeuronalGPI-Linked ProteinsInflammation MediatorsL-Lactate DehydrogenaseSEMA7A protein, humanSemaphorins

Identifiers

PMID26963322
OpenAlexW2325634249

What OpenQuestion holds

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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.