Evidence map›Paper›PMID 22019898›Full record

ArticleThe American journal of pathology2011

The protective role of CD59 and pathogenic role of complement in hepatic ischemia and reperfusion injury.

Jinyan Zhang, Weiguo Hu, Wei Xing, Tao You, Junming Xu, Xuebin Qin, Zhihai Peng

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.7field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Dihydro-stilbene gigantol relieves CClActa pharmacologica Sinica · 2020
    Article
  9. Review
  10. Onset of Donor Warm Ischemia Time in Donation After Circulatory Death Liver Transplantation: Hypotension or Hypoxia?Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Use of a hanging-weight system for liver ischemia in mice.Journal of visualized experiments : JoVE · 2012
    Article
  18. Review
  19. 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

7 authors at 5 institutions in 2 countries.

Jinyan ZhangDepartment of General Surgery, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai, China.
Weiguo Hu
Wei Xing
Tao You
Junming Xu
Xuebin Qin
Zhihai Peng
Brigham and Women's Hospital · USShanghai First People's Hospital · CNCenter for Rheumatology · USENT and Allergy · USHarvard University · US

Funding

Towards a Mouse Model of Complement-Mediated DiseasesR01AI061174 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI QIN, XUEBIN · 2005 to 2009
$1.8M
NIAID NIH HHS R01 AI061174
6 · The paper itself

Abstract

Hepatic ischemia-reperfusion injury (IRI) is a major factor influencing graft outcome in liver transplantation, but its mechanism is not well defined. Although complement, including the membrane attack complex (MAC), a terminal product of complement activation, is thought to be involved in the multiple reactions subsequent to the ischemia-reperfusion (IR) process, the role of MAC in the pathogenesis of hepatic IRI requires further investigation. We used a warm ischemia-reperfusion injury model in mice and a syngeneic orthotopic liver transplantation model in rats to define the role of complement, including MAC, in hepatic IR. CD59-deficient mice had more severe liver dysfunction, evidenced by increased aspartate aminotransferase levels and increased injury of liver parenchymal and nonparenchymal cells than did CD59-sufficient mice during warm hepatic IR. Furthermore, complement depletion in CD59-deficient mice by pretreatment with cobra venom factor (CVF) or the genetic introduction of C3 deficiency partially protected against development of the severe liver dysfunction that occurred in CD59-deficient mice. Severity of liver dysfunction correlated with MAC deposition, apoptotic cells, and increased inflammatory mediators such as tumor necrosis factor α. Moreover, depletion of complement with CVF in orthotopic liver transplantation recipient rats attenuated IRI of the donor livers. Taken together, these results highlight the protective role of CD59 and pathogenic role of complement, including MAC, in the pathogenesis of hepatic IRI.

Indexed as

Alanine TransaminaseAnimalsApoptosisAspartate AminotransferasesCD59 AntigensCell LineComplement ActivationComplement C3Complement Inactivating AgentsComplement Membrane Attack ComplexCytokinesElapid VenomsGraft SurvivalLiverLiver DiseasesLiver TransplantationAlanine TransaminaseAspartate AminotransferasesCD59 Antigenscobra venom factorComplement C3Complement Inactivating AgentsComplement Membrane Attack ComplexCytokinesElapid Venoms

Identifiers

PMID22019898
PMCPMC3260856
OpenAlexW2024203095

What OpenQuestion holds

Textmetadata
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.