Evidence map›Paper›PMID 26683513›Full record

ArticleTransplantation2016

The Dichotomy of Endoplasmic Reticulum Stress Response in Liver Ischemia-Reperfusion Injury.

Haomming Zhou, Jianjun Zhu, Shi Yue, Ling Lu, Ronald W Busuttil, Jerzy W Kupiec-Weglinski, Xuehao Wang, Yuan Zhai

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Transplantation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Dietary SupplementOxidative medicine and cellular longevity · 2021
    Article
  8. Article
  9. Article
  10. Article
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  13. Review
  14. Article
  15. Article
  16. Endoplasmic reticulum stress and liver diseases.Liver research (Beijing, China) · 2019
    Article
  17. Review
  18. Article
  19. Article
  20. Review
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

8 authors at 1 institution in 1 country.

Haomming Zhou1 Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China. 2 Dumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA. 3 Department of Liver Surgery, Renji Hospital, Shanghai Jiaotong University, Shanghai, China.
Jianjun Zhu
Shi Yue
Ling Lu
Ronald W Busuttil
Jerzy W Kupiec-Weglinski
Xuehao Wang
Yuan Zhai
Renji Hospital · CN

Funding

CXCL10/CXCR3 Signaling Regulates TLR4-Mediated Liver Inflamation and InjuryR01DK083408 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHAI, YUAN · 2010 to 2014
$1.6M
Kupffer Cell Necroptosis and Homeostatic Function in Liver Immune Responses against Ischemia Reperfusion InjuryR21AI126516 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHAI, YUAN · 2016 to 2017
$424k
NIAID NIH HHS R21 AI126516NIDDK NIH HHS R01 DK083408
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress plays critical roles in the pathogenesis of liver ischemia-reperfusion injury (IRI). As ER stress triggers an adaptive cellular response, the question of what determines its functional outcome in liver IRI remains to be defined. In a murine liver partial warm ischemia model, we studied how transient (30 minutes) or prolonged (90 minutes) liver ischemia regulated local ER stress response and autophagy activities and their relationship with liver IRI. Effects of chemical chaperon 4-phenylbutyrate (4-PBA) or autophagy inhibitor 3-methyladenine (3-MA) were evaluated. Our results showed that although the activating transcription factor 6 branch of ER stress response was induced in livers by both types of ischemia, liver autophagy was activated by transient, but inhibited by prolonged, ischemia. Although 3-MA had no effects on liver IRI after prolonged ischemia, it significantly increased liver IRI after transient ischemia. The 4-PBA treatment protected livers from IRI after prolonged ischemia by restoring autophagy flux, and the adjunctive 3-MA treatment abrogated its liver protective effect. The same 4-PBA treatment, however, increased liver IRI and disrupted autophagy flux after transient ischemia. Although both types of ischemia activated 5' adenosine monophosphate-activated protein kinase and inactivated protein kinase B (Akt), prolonged ischemia also resulted in downregulations of autophagy-related gene 3 and autophagy-related gene 5 in ischemic livers. These results indicate a functional dichotomy of ER stress response in liver IRI via its regulation of autophagy. Transient ischemia activates autophagy to protect livers from IRI, whereas prolonged ischemia inhibits autophagy to promote the development of liver IRI.

Indexed as

AutophagyEndoplasmic Reticulum StressActivating Transcription FactorsAdenineAMP-Activated Protein KinasesAnimalsAutophagy-Related Protein 5Autophagy-Related ProteinsDisease Models, AnimalEndoplasmic ReticulumLiverLiver DiseasesMaleMice, Inbred C57BLMicrotubule-Associated ProteinsPhenylbutyrates3-methyladenine4-phenylbutyric acidActivating Transcription FactorsAdenineAMP-Activated Protein KinasesAtf5 protein, mouseAtg3 protein, mouseAtg5 protein, mouseAutophagy-Related Protein 5Autophagy-Related ProteinsMicrotubule-Associated ProteinsPhenylbutyratesProto-Oncogene Proteins c-aktUbiquitin-Conjugating Enzymes

Identifiers

PMID26683513
PMCPMC4731254
OpenAlexW2308775225

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.