Evidence map›Paper›PMID 31718093›Full record

ArticleCells2019

Augmenter of Liver Regeneration Reduces Ischemia Reperfusion Injury by Less Chemokine Expression, Gr-1 Infiltration and Oxidative Stress.

Thomas S Weiss, Madeleine Lupke, Rania Dayoub, Edward K Geissler, Hans J Schlitt, Michael Melter, Elke Eggenhofer

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. 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
1.8field-weighted citation impact, top 15% 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.

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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

7 authors at 1 institution in 1 country.

Thomas S WeissUniversity Children Hospital (KUNO), University Hospital Regensburg, 93053 Regensburg, Germany.ORCID 0000-0003-0336-0581
Madeleine LupkeUniversity Children Hospital (KUNO), University Hospital Regensburg, 93053 Regensburg, Germany.
Rania DayoubUniversity Children Hospital (KUNO), University Hospital Regensburg, 93053 Regensburg, Germany.ORCID 0000-0001-5848-5571
Edward K GeisslerDepartment of Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
Hans J SchlittDepartment of Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
Michael MelterUniversity Children Hospital (KUNO), University Hospital Regensburg, 93053 Regensburg, Germany.
Elke EggenhoferDepartment of Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.
University Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic ischemia reperfusion injury (IRI) is a major complication in liver resection and transplantation. Here, we analyzed the impact of recombinant human augmenter of liver regeneration (rALR), an anti-oxidative and anti-apoptotic protein, on the deleterious process induced by ischemia reperfusion (IR). Application of rALR reduced tissue damage (necrosis), levels of lipid peroxidation (oxidative stress) and expression of anti-oxidative genes in a mouse IRI model. Damage associated molecule pattern (DAMP) and inflammatory cytokines such as HMGB1 and TNFα, were not affected by rALR. Furthermore, we evaluated infiltration of inflammatory cells into liver tissue after IRI and found no change in CD3 or γδTCR positive cells, or expression of IL17/IFNγ by γδTCR cells. The quantity of Gr-1 positive cells (neutrophils), and therefore, myeloperoxidase activity, was lower in rALR-treated mice. Moreover, we found under hypoxic conditions attenuated ROS levels after ALR treatment in RAW264.7 cells and in primary mouse hepatocytes. Application of rALR also led to reduced expression of chemo-attractants like CXCL1, CXCL2 and CCl2 in hepatocytes. In addition, ALR expression was increased in IR mouse livers after 3 h and in biopsies from human liver transplants with minimal signs of tissue damage. Therefore, ALR attenuates IRI through reduced neutrophil tissue infiltration mediated by lower expression of key hepatic chemokines and reduction of ROS generation.

Indexed as

Oxidative StressAnimalsAntigens, LyApoptosisBiopsyChemokinesDisease Models, AnimalFlow CytometryHepatocytesImmunohistochemistryLiverLiver RegenerationMaleMiceModels, BiologicalNeutrophilsAntigens, LyChemokinesReactive Oxygen Speciesaugmenter of liver regenerationchemokinesischemia reperfusionliver regenerationneutrophilsoxidative stress

Identifiers

PMID31718093
PMCPMC6912457
OpenAlexW2985879981

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.