Evidence map›Paper›PMID 23435964›Full record

ArticleApoptosis : an international journal on programmed cell death2013

Induction of heme oxygenase-1 protects mouse liver from apoptotic ischemia/reperfusion injury.

Z Ben-Ari, Y Issan, Y Katz, M Sultan, M Safran, Laniado-Schwartzman Michal, G Abraham Nader, R Kornowski, F Grief, O Pappo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Transduced PEP-1-heme oxygenase-1 fusion protein reduces remote organ injury induced by intestinal ischemia/reperfusion.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  10. Protective role of hemeoxygenase-1 in gastrointestinal diseases.Cellular and molecular life sciences : CMLS · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

11 authors at 6 institutions in 2 countries.

Z Ben-AriLiver Disease Center, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel. ziv.ben-ari@sheba.health.gov.il
Y Issan
Y Katz
M Sultan
M Safran
Laniado-Schwartzman Michal
G Abraham Nader
R Kornowski
F Grief
O Pappo
E Hochhauser
Rabin Medical Center · ILCalifornia Liver Research Institute · USTel Aviv University · ILMarshall University · USNew York Medical College · USSheba Medical Center · IL

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI JIANG, HOULI · 1985 to 2015
$33.4M
NHLBI NIH HHS P01 HL034300
6 · The paper itself

Abstract

Ischemia/reperfusion (I/R) injury is the main cause of primary graft dysfunction of liver allografts. Cobalt-protoporphyrin (CoPP)-dependent induction of heme oxygenase (HO)-1 has been shown to protect the liver from I/R injury. This study analyzes the apoptotic mechanisms of HO-1-mediated cytoprotection in mouse liver exposed to I/R injury. HO-1 induction was achieved by the administration of CoPP (1.5 mg/kg body weight i.p.). Mice were studied in in vivo model of hepatic segmental (70 %) ischemia for 60 min and reperfusion injury. Mice were randomly allocated to four main experimental groups (n = 10 each): (1) A control group undergoing sham operation. (2) Similar to group 1 but with the administration of CoPP 72 h before the operation. (3) Mice undergoing in vivo hepatic I/R. (4) Similar to group 3 but with the administration of CoPP 72 h before ischemia induction. When compared with the I/R mice group, in the I/R+CoPP mice group, the increased hepatic expression of HO-1 was associated with a significant reduction in liver enzyme levels, fewer apoptotic hepatocytes cells were identified by morphological criteria and by immunohistochemistry for caspase-3, there was a decreased mean number of proliferating cells (positively stained for Ki67), and a reduced hepatic expression of: C/EBP homologous protein (an index of endoplasmic reticulum stress), the NF-κB's regulated genes (CIAP2, MCP-1 and IL-6), and increased hepatic expression of IκBa (the inhibitory protein of NF-κB). HO-1 over-expression plays a pivotal role in reducing the hepatic apoptotic IR injury. HO-1 may serve as a potential target for therapeutic intervention in hepatic I/R injury during liver transplantation.

Indexed as

AnimalsApoptosisBiomarkersCaspase 3CCAAT-Enhancer-Binding ProteinsCytoprotectionEnzyme InductionGene ExpressionHeme Oxygenase-1HepatocytesInhibitor of Apoptosis ProteinsInjections, IntraperitonealKi-67 AntigenLiverMaleMembrane ProteinsBiomarkersCasp3 protein, mouseCaspase 3CCAAT-Enhancer-Binding ProteinscobaltiprotoporphyrinHeme Oxygenase-1Hmox1 protein, mouseInhibitor of Apoptosis ProteinsKi-67 AntigenMembrane ProteinsProtoporphyrins

Identifiers

PMID23435964
PMCPMC5560494
OpenAlexW2034437306

What OpenQuestion holds

Textmetadata
LicenceTDM
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.