Evidence map›Paper›PMID 27713143›Full record

ArticleOncotarget2016

Signaling through hepatocyte vasopressin receptor 1 protects mouse liver from ischemia-reperfusion injury.

Xiqiang Liu, Gaojian Luo, Jingbo Jiang, Tonghui Ma, Xiaozhu Lin, Liping Jiang, Jilin Cheng, Ran Tao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  4. Review
  5. Review
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  8. Neuroprotective Effect of Aurantio-Obtusin, a Putative Vasopressin VInternational journal of molecular sciences · 2021
    Article
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  11. Review
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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

8 authors at 5 institutions in 1 country.

Xiqiang LiuDepartment of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital (ZJPPH), Hangzhou, Zhejiang, PR China.
Gaojian LuoDepartment of General Surgery, Affiliated Yiwu Hospital, Wenzhou Medical University, Yiwu, Zhejiang, PR China.
Jingbo JiangDepartment of Surgery, Qilu Hospital, Shandong University School of Medicine, Jinan, Shandong, PR China.
Tonghui MaDepartment of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital (ZJPPH), Hangzhou, Zhejiang, PR China.
Xiaozhu LinDepartment of Radiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.
Liping JiangDepartment of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital (ZJPPH), Hangzhou, Zhejiang, PR China.
Jilin ChengDepartment of Gastroenterology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, PR China.
Ran TaoDepartment of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital (ZJPPH), Hangzhou, Zhejiang, PR China.
Zhejiang Provincial People's Hospital · CNQilu Hospital of Shandong University · CNRuijin Hospital · CNShanghai Public Health Clinical Center · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Terlipressin has been used extensively in the management of certain complications associated with end-stage liver diseases (ESLDs). In our pilot study, terlipressin treatment showed beneficial effects on liver function in patients with decompensated cirrhosis, however whether it plays a role in liver ischemia-reperfusion injury (IRI) remains unknown. Using a mouse nonlethal hepatic IR model, we found terlipressin administration significantly ameliorated IR-induced liver apoptosis, necrosis and inflammation. Furthermore, despite its known effect on visceral vasoconstriction, hemodynamic evaluation of murine hepatic tissue after IR revealed no change of overall hepatic blood flow after terlipressin treatment. Further studies identified the upregulation of vasopressin receptor 1 (V1R) expression on hepatocytes upon IR. In isolated hepatocyte hypoxia/reoxygenation model, the active component of terlipressin, lysine vasopressin, conferred hepatocytes resistant to oxidative stress-induced apoptosis. Mechanistic studies revealed the V1R engagement activated the Wnt/β-catenin/FoxO3a/AKT pathway, which subsequently circumvented the proapoptotic events, thus ameliorated hepatocyte apoptosis. Furthermore, genetic knockdown of V1R expression in hepatocyte cell lines or blockade of this signaling pathway abrogated such protective effect.

conclusionThese data highlight the functional importance of the hepatocyte V1R/Wnt/β-catenin/FoxO3a/AKT pathway in protecting liver from oxidative stress-induced injury.

Indexed as

AnimalsApoptosisCytoprotectionForkhead Box Protein O3HepatocytesHumansLiverLypressinMaleMice, Inbred C57BLProto-Oncogene Proteins c-aktReceptors, VasopressinReperfusion InjuryRNA InterferenceSignal TransductionVasoconstrictor AgentsForkhead Box Protein O3FoxO3 protein, mouseLypressinProto-Oncogene Proteins c-aktReceptors, VasopressinVasoconstrictor AgentsapoptosishepatocytehypoxiainflammationPathology Sectionvasopressin receptor

Identifiers

PMID27713143
PMCPMC5342477
OpenAlexW2529713020

What Socratic 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 Socratic graph.