Evidence map›Paper›PMID 30175514›Full record

ArticleNephrology (Carlton, Vic.)2019

Loss of receptor interacting protein kinases 3 and caspase-8 augments intrinsic apoptosis in tubular epithelial cell and promote kidney ischaemia-reperfusion injury.

Baekjun Sung, Ye Su, Jifu Jiang, Patrick Mcleod, Weihua Liu, Aaron Haig, Douglas R Green, Zhu-Xu Zhang, Anthony M Jevnikar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nephrology (Carlton, Vic.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 countries.

Baekjun SungLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
Ye SuLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
Jifu JiangLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
Patrick McleodLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
Weihua LiuDepartment of Pathology, Western University, London, Ontario, Canada.
Aaron HaigDepartment of Pathology, Western University, London, Ontario, Canada.
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Zhu-Xu ZhangLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
Anthony M JevnikarLondon Health Sciences Centre University Hospital, Matthew Mailing Centre for Translational Transplantation Studies, London, Ontario, Canada.
London Health Sciences Centre · CAWestern University · CASt. Jude Children's Research Hospital · US

Funding

Survival Function of the Fadd-Caspase-8-Flip ComplexR01AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GREEN, DOUGLAS R. · 1999 to 2016
$6.3M
Survival Function of the Fadd-Caspase-8-Flip Complex - MERIT ExtensionR37AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2017 to 2026
$4.5M
Canadian National Transplant Research Program TFU-127880CIHR MOP-111180, MOP-115048Kidney Foundation of Canada KFOC160020NIAID NIH HHS R01 AI044828NIAID NIH HHS R37 AI044828
6 · The paper itself

Abstract

backgroundIschaemia-reperfusion injury (IRI) is associated with programmed cell death that promotes inflammation and organ dysfunction. Necroptosis is mediated by members of receptor interacting protein kinases (RIPK1/3). Inhibition of RIPK1/3 provides a pro-survival benefit in kidney IRI. Caspase-8 initiates apoptosis and contributes to IRI. We studied whether inhibiting both RIPK3 and caspase-8 would provide an additional benefit in kidney IRI.

methodsA clamp was applied to the left kidney pedicle for 45 min followed by right kidney nephrectomy. Kidney and serum from wild type, RIPK3

resultsKidney IRI of DKO mice did not show improvement over RIPK3

conclusionWe show that the deletion of both RIPK3 and caspase-8 does not provide additive benefit in IRI or TEC death and may enhance injury by up-regulation of intrinsic apoptosis. This suggests blocking multiple death pathways may be required for the prevention of kidney IRI clinically.

Indexed as

ApoptosisAnimalsCaspase 8Disease Models, AnimalEpithelial CellsInterferon-gammaInterleukin-1betaKidney DiseasesKidney TubulesMaleMiceMice, Inbred C57BLMice, KnockoutNecroptosisNIH 3T3 CellsReceptor-Interacting Protein Serine-Threonine KinasesCasp8 protein, mouseCaspase 8IFNG protein, mouseIL1B protein, mouseInterferon-gammaInterleukin-1betaReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseapoptosiscaspase-8ischaemia-reperfusion injurykidneynecroptosisreceptor interacting protein kinases 3

Identifiers

PMID30175514
PMCPMC7706480
OpenAlexW2892064423

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.