Evidence map›Paper›PMID 26451593›Full record

ArticlePloS one2015

Mitochondrial Damage-Associated Molecular Patterns (MTDs) Are Released during Hepatic Ischemia Reperfusion and Induce Inflammatory Responses.

Qianni Hu, Caroline Ruth Wood, Sanem Cimen, Ananda Baskaran Venkatachalam, Ian Patrick Joseph Alwayn

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Article
  2. Review
  3. Biomedicines · 2026
    Article
  4. Neutrophil-T cell cross talk in noninfectious liver diseases.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. [Research Progress on the Role of Mitochondrial DNA in the Pathogenesis of Chronic Liver Disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Article
  18. Review
  19. Article
  20. Article
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

5 authors.

Qianni HuDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
Caroline Ruth WoodDepartment of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
Sanem CimenDepartment of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
Ananda Baskaran VenkatachalamDepartment of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
Ian Patrick Joseph AlwaynDepartments of Surgery, Pathology, Microbiology & Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.

Funding

University of Cincinnati-Marietta-Parkersburg Metropolitan Area Reciprocal ResearR03ES017362 · NIEHS · UNIVERSITY OF CINCINNATI · PI HAYNES, ERIN N · 2008 to 2009
$125k
CIHR RES0017362NIEHS NIH HHS R03 ES017362
6 · The paper itself

Abstract

Ischemia / reperfusion injury (IRI) during the course of liver transplantation enhances the immunogenicity of allografts and thus impacts overall graft outcome. This sterile inflammatory insult is known to activate innate immunity and propagate organ damage through the recognition of damage-associate molecular pattern (DAMP) molecules. The purpose of the present study was to investigate the role of mitochondrial DAMPs (MTDs) in the pathogenesis of hepatic IRI. Using in vitro models we observed that levels of MTDs were significantly higher in both transplantation-associated and warm IR, and that co-culture of MTDs with human and rat hepatocytes significantly increased cell death. MTDs were also released in an in vivo rat model of hepatic IRI and associated with increased secretion of inflammatory cytokines (TNF-α, IL-6, and IL-10) and increased liver injury compared to the sham group. Our results suggest that hepatic IR results in a significant increase of MTDs both in vitro and in vivo suggesting that MTDs may serve as a novel marker in hepatic IRI. Co-culture of MTDs with hepatocytes showed a decrease in cell viability in a concentration dependent manner, which indicates that MTDs is a toxic mediator participating in the pathogenesis of liver IR injury.

Indexed as

Liver TransplantationAnimalsApoptosisBiomarkersCell LineCell SurvivalCoculture TechniquesCytokinesDNA, MitochondrialHepatocytesHumansInflammationIschemiaLiverMaleMitochondriaBiomarkersCytokinesDNA, Mitochondrial

Identifiers

PMID26451593
PMCPMC4599831

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Registered trials

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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.