Evidence map›Paper›PMID 34681708›Full record

ArticleInternational journal of molecular sciences2021

Cyclophilin D Regulates the Nuclear Translocation of AIF, Cardiac Endothelial Cell Necroptosis and Murine Cardiac Transplant Injury.

Adnan Qamar, Jianqi Zhao, Laura Xu, Patrick McLeod, Xuyan Huang, Jifu Jiang, Weihua Liu, Aaron Haig, Zhu-Xu Zhang

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

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 14 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

9 authors at 2 institutions in 2 countries.

Adnan QamarMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Jianqi ZhaoMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Laura XuMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Patrick McLeodMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Xuyan HuangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Jifu JiangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.
Weihua LiuDepartment of Pathology, Western University, 1151 Richmond Street, London, ON N6A 3K7, Canada.
Aaron HaigDepartment of Pathology, Western University, 1151 Richmond Street, London, ON N6A 3K7, Canada.
Zhu-Xu ZhangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, B4-231, 339 Windermere Road, London, ON N6A 5A5, Canada.ORCID 0000-0002-8335-3738
Western University · CALondon Health Sciences Centre · CA

Funding

Canadian Institutes of Health Research FRN169045
6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is an inevitable consequence of organ transplant procedure and associated with acute and chronic organ rejection in transplantation. IRI leads to various forms of programmed cell death, which worsens tissue damage and accelerates transplant rejection. We recently demonstrated that necroptosis participates in murine cardiac microvascular endothelial cell (MVEC) death and murine cardiac transplant rejection. However, MVEC death under a more complex IRI model has not been studied. In this study, we found that simulating IRI conditions in vitro by hypoxia, reoxygenation and treatment with inflammatory cytokines induced necroptosis in MVECs. Interestingly, the apoptosis-inducing factor (AIF) translocated to the nucleus during MVEC necroptosis, which is regulated by the mitochondrial permeability molecule cyclophilin D (CypD). Furthermore, CypD deficiency in donor cardiac grafts inhibited AIF translocation and mitigated graft IRI and rejection (

Indexed as

NecroptosisAnimalsApoptosis Inducing FactorCell HypoxiaCell NucleusEndothelial CellsInterferon-gammaMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMicrovesselsModels, BiologicalOxygenPeptidyl-Prolyl Isomerase FReceptor-Interacting Protein Serine-Threonine KinasesApoptosis Inducing FactorInterferon-gammaOxygenPeptidyl-Prolyl Isomerase FReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseRNA, Small InterferingTumor Necrosis Factor-alphaAIFcardiacCypDendothelial cellhypoxiaischemianecroptosistransplantation

Identifiers

PMID34681708
PMCPMC8540562
OpenAlexW3207730806

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.