Evidence map›Paper›PMID 29364854›Full record

ArticleInternational journal of molecular sciences2018

Cytoprotective Mechanisms in Fatty Liver Preservation against Cold Ischemia Injury: A Comparison between IGL-1 and HTK.

Arnau Panisello-Roselló, Eva Verde, Alexandre Lopez, Marta Flores, Emma Folch-Puy, Anabela Rolo, Carlos Palmeira, Georgina Hotter, Teresa Carbonell, René Adam and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  10. Article
  11. Review
  12. Article
  13. Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury.International journal of molecular sciences · 2018
    Article
  14. Aldehyde Dehydrogenase 2 (ALDH2) in Rat Fatty Liver Cold Ischemia Injury.International journal of molecular sciences · 2018
    Article
  15. Review
  16. Review
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

11 authors at 4 institutions in 3 countries.

Arnau Panisello-RosellóExperimental Hepatic Ischemia-Reperfusion Unit, Institut d'Investigacions Biomèdiques de Barcelona (IIBB), Spanish National Research Council (CSIC), 08036 Barcelona, Catalonia, Spain. arnau.panisello.rosello@gmail.com.
Eva VerdeDepartment of Cell Biology, Physiology and Immunology, Universitat de Barcelona, Barcelona, 08028 Catalonia, Spain. e.vaaverde@gmail.com.
Alexandre LopezCentre Hépato-Biliaire, AP-PH, Hôpital Paul Brousse, 94800 Villejuif, France. alexandregl.lopez@gmail.com.ORCID 0000-0001-8978-4486
Marta FloresDepartment of Cell Biology, Physiology and Immunology, Universitat de Barcelona, Barcelona, 08028 Catalonia, Spain. mfloreso10@alumnes.ub.edu.
Emma Folch-PuyExperimental Hepatic Ischemia-Reperfusion Unit, Institut d'Investigacions Biomèdiques de Barcelona (IIBB), Spanish National Research Council (CSIC), 08036 Barcelona, Catalonia, Spain. emma.folch@iibb.csic.es.
Anabela RoloCenter for Neuroscience and Cell Biology, Universidade Coimbra, 3000-370 Coimbra, Portugal. anpiro@ci.uc.pt.
Carlos PalmeiraCenter for Neuroscience and Cell Biology, Universidade Coimbra, 3000-370 Coimbra, Portugal. palmeira@uc.pt.
Georgina HotterExperimental Hepatic Ischemia-Reperfusion Unit, Institut d'Investigacions Biomèdiques de Barcelona (IIBB), Spanish National Research Council (CSIC), 08036 Barcelona, Catalonia, Spain. ghcbam@iibb.csic.es.
Teresa CarbonellDepartment of Cell Biology, Physiology and Immunology, Universitat de Barcelona, Barcelona, 08028 Catalonia, Spain. tcarbonell@ub.edu.ORCID 0000-0002-7131-3667
René AdamCentre Hépato-Biliaire, AP-PH, Hôpital Paul Brousse, 94800 Villejuif, France. rene.adam@aphp.fr.
Joan Roselló-CatafauExperimental Hepatic Ischemia-Reperfusion Unit, Institut d'Investigacions Biomèdiques de Barcelona (IIBB), Spanish National Research Council (CSIC), 08036 Barcelona, Catalonia, Spain. jrcbam@iibb.csic.es.
Consejo Superior de Investigaciones Científicas · ESUniversitat de Barcelona · ESCentro de Neurociências e Biologia Celular · PTHôpital Paul-Brousse · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Institute Goeorges Lopez 1 (IGL-1) and Histidine-Tryptophan-Ketoglutarate (HTK) preservation solutions are regularly used in clinical for liver transplantation besides University of Wisconsin (UW) solution and Celsior. Several clinical trials and experimental works have been carried out comparing all the solutions, however the comparative IGL-1 and HTK appraisals are poor; especially when they deal with the underlying protection mechanisms of the fatty liver graft during cold storage. Fatty livers from male obese Zücker rats were conserved for 24 h at 4 °C in IGL-1 or HTK preservation solutions. After organ recovery and rinsing of fatty liver grafts with Ringer Lactate solution, we measured the changes in mechanistic target of rapamycin (mTOR) signaling activation, liver autophagy markers (Beclin-1, Beclin-2, LC3B and ATG7) and apoptotic markers (caspase 3, caspase 9 and TUNEL). These determinations were correlated with the prevention of liver injury (aspartate and alanine aminostransferase (AST/ALT), histology) and mitochondrial damage (glutamate dehydrogenase (GLDH) and confocal microscopy findings). Liver grafts preserved in IGL-1 solution showed a marked reduction on p-TOR/mTOR ratio when compared to HTK. This was concomitant with significant increased cyto-protective autophagy and prevention of liver apoptosis, including inflammatory cytokines such as HMGB1. Together, our results revealed that IGL-1 preservation solution better protected fatty liver grafts against cold ischemia damage than HTK solution. IGL-1 protection was associated with a reduced liver damage, higher induced autophagy and decreased apoptosis. All these effects would contribute to limit the subsequent extension of reperfusion injury after graft revascularization in liver transplantation procedures.

Indexed as

Cold IschemiaCytoprotectionOrgan PreservationAnimalsApoptosisAutophagyBiomarkersCryopreservationFatty LiverGene ExpressionGlucoseHistocytochemistryHMGB1 ProteinLiver Function TestsLiver TransplantationMaleBiomarkersBretschneider cardioplegic solutionGlucoseHMGB1 ProteinIGL-1 solutionMannitolOrgan Preservation SolutionsPotassium ChlorideProcaineTOR Serine-Threonine Kinasesautophagy and apoptosiscold ischemia injuryHTK solutionIGL-1 solutionlivermTOR

Identifiers

PMID29364854
PMCPMC5855570
OpenAlexW2785496833

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.