Evidence map›Paper›PMID 20730776›Full record

ArticleHepatology (Baltimore, Md.)2010

Growth arrest-specific protein 6 is hepatoprotective against murine ischemia/reperfusion injury.

Laura Llacuna, Cristina Bárcena, Lola Bellido-Martín, Laura Fernández, Milica Stefanovic, Montserrat Marí, Carmen García-Ruiz, José C Fernández-Checa, Pablo García de Frutos, Albert Morales

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. GAS6/Axl is associated with AMPK activation and attenuates HApoptosis : an international journal on programmed cell death · 2023
    Article
  15. Article
  16. Review
  17. Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022
    Review
  18. Review
  19. Review
  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

10 authors at 2 institutions in 3 countries.

Laura LlacunaLiver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer/Centre d'Investigació Biomèdica Esther Koplowitz, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Barcelona, Spain.
Cristina Bárcena
Lola Bellido-Martín
Laura Fernández
Milica Stefanovic
Montserrat Marí
Carmen García-Ruiz
José C Fernández-Checa
Pablo García de Frutos
Albert Morales
Consejo Superior de Investigaciones Científicas · ESUniversity of Southern California · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50 AA 11999
6 · The paper itself

Abstract

unlabelledGrowth arrest-specific gene 6 (GAS6) promotes growth and cell survival during tissue repair and development in different organs, including the liver. However, the specific role of GAS6 in liver ischemia/reperfusion (I/R) injury has not been previously addressed. Here we report an early increase in serum GAS6 levels after I/R exposure. Moreover, unlike wild-type (WT) mice, Gas6(-/-) mice were highly sensitive to partial hepatic I/R, with 90% of the mice dying within 12 hours of reperfusion because of massive hepatocellular injury. I/R induced early hepatic protein kinase B (AKT) phosphorylation in WT mice but not in Gas6(-/-) mice without significant changes in c-Jun N-terminal kinase phosphorylation or nuclear factor kappa B translocation, whereas hepatic interleukin-1β (IL-1β) and tumor necrosis factor (TNF) messenger RNA levels were higher in Gas6(-/-) mice versus WT mice. In line with the in vivo data, in vitro studies indicated that GAS6 induced AKT phosphorylation in primary mouse hepatocytes and thus protected them from hypoxia-induced cell death, whereas GAS6 diminished lipopolysaccharide-induced cytokine expression (IL-1β and TNF) in murine macrophages. Finally, recombinant GAS6 treatment in vivo not only rescued GAS6 knockout mice from severe I/R-induced liver damage but also attenuated hepatic damage in WT mice after I/R.

conclusionOur data have revealed GAS6 to be a new player in liver I/R injury that is emerging as a potential therapeutic target for reducing postischemic hepatic damage.

Indexed as

AnimalsGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsInterleukin-1betaJNK Mitogen-Activated Protein KinasesLiver DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutPhosphorylationProto-Oncogene Proteins c-aktReperfusion InjuryRNA, MessengerTumor Necrosis Factor-alphaGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsInterleukin-1betaJNK Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID20730776
PMCPMC2947564
OpenAlexW2130636524

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.