Evidence map›Paper›PMID 25445398›Full record

ArticleJournal of hepatology2015

TRAIL receptor deletion in mice suppresses the inflammation of nutrient excess.

Leila Idrissova, Harmeet Malhi, Nathan W Werneburg, Nathan K LeBrasseur, Steven F Bronk, Christian Fingas, Tamar Tchkonia, Tamar Pirtskhalava, Thomas A White, Michael B Stout and 8 more

Abstract read
In one paragraph

Article in Journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 91 citations in OpenAlex.

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  17. Nonalcoholic Steatohepatitis Promoting Kinases.Seminars in liver disease · 2020
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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

18 authors at 4 institutions in 2 countries.

Leila IdrissovaDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Harmeet MalhiDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States. Electronic address: malhi.harmeet@mayo.edu.
Nathan W WerneburgDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Steven F BronkDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Christian FingasDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Tamar TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Tamar PirtskhalavaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Thomas A WhiteRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Michael B StoutRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Petra HirsovaDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Anuradha KrishnanDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States.
Christian LiedtkeDepartment of Medicine III, University Hospital, Aachen, Germany.
Christian TrautweinDepartment of Medicine III, University Hospital, Aachen, Germany.
Niklas FinnbergPenn State Hershey Cancer Institute, Hershey, PA 17033, United States.
Wafik S El-DeiryPenn State Hershey Cancer Institute, Hershey, PA 17033, United States.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, United States.
Gregory J GoresDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, United States. Electronic address: gores.gregory@mayo.edu.
Mayo Clinic in Arizona · USMayo Clinic in Florida · USPenn State Milton S. Hershey Medical Center · USUniversitätsklinikum Aachen · DE

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Effect of Aging on Preadipocyte DifferentiationR01AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 1997 to 2012
$3.7M
MECHANISMS OF LIVER CELL INJURYR01DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 1992 to 2019
$3.6M
MECHANISMS OF LIVER CELL INJURYR37DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2000 to 2009
$2.9M
Mechanisms of Liver InflammationK08DK097178 · NIDDK · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET · 2012 to 2016
$730k
INTRACELLULAR PH IN LIVER CELL INJURYR29DK041876 · NIDDK · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GORES, GREGORY J. · 1989 to 1992
–
NIA NIH HHS AG13925NIA NIH HHS P01 AG041122NIA NIH HHS R01 AG013925NIA NIH HHS R37 AG013925NIDDK NIH HHS DK41876NIDDK NIH HHS DK50456NIDDK NIH HHS DK97178NIDDK NIH HHS K08 DK097178NIDDK NIH HHS P30 DK050456NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK041876NIDDK NIH HHS R37 DK041876
6 · The paper itself

Abstract

BACKGROUND &

aimsLow-grade chronic inflammation is a cardinal feature of the metabolic syndrome, yet its pathogenesis is not well defined. The purpose of this study was to examine the role of TRAIL receptor (TR) signaling in the pathogenesis of obesity-associated inflammation using mice with the genetic deletion of TR.

methodsTR knockout (TR(-/-)) mice and their littermate wild-type (WT) mice were fed a diet high in saturated fat, cholesterol and fructose (FFC) or chow. Metabolic phenotyping, liver injury, and liver and adipose tissue inflammation were assessed. Chemotaxis and activation of mouse bone marrow-derived macrophages (BMDMϕ) was measured.

resultsGenetic deletion of TR completely repressed weight gain, adiposity and insulin resistance in FFC-fed mice. Moreover, TR(-/-) mice suppressed steatohepatitis, with essentially normal serum ALT, hepatocyte apoptosis and liver triglyceride accumulation. Gene array data implicated inhibition of macrophage-associated hepatic inflammation in the absence of the TR. In keeping with this, there was diminished accumulation and activation of inflammatory macrophages in liver and adipose tissue. TR(-/-) BMDMϕ manifest reduced chemotaxis and diminished activation of nuclear factor-κ B signaling upon activation by palmitate and lipopolysaccharide.

conclusionsThese data advance the concept that macrophage-associated hepatic and adipose tissue inflammation of nutrient excess requires TR signaling.

Indexed as

Adipose TissueInflammationLiverMacrophagesObesityReceptors, TNF-Related Apoptosis-Inducing LigandAnimalsChemotaxisDiet, High-FatDisease Models, AnimalMacrophage ActivationMiceMice, KnockoutSignal TransductionReceptors, TNF-Related Apoptosis-Inducing LigandLipoapoptosisMacrophage activationMetainflammationNon-alcoholic fatty liver disease

Identifiers

PMID25445398
PMCPMC4404200
OpenAlexW2004933414

What OpenQuestion holds

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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.