Evidence map›Paper›PMID 27941027›Full record

ArticleJournal of lipid research2017

The lipid droplet-associated protein perilipin 3 facilitates hepatitis C virus-driven hepatic steatosis.

Daniel Ferguson, Jun Zhang, Matthew A Davis, Robert N Helsley, Lise-Lotte Vedin, Richard G Lee, Rosanne M Crooke, Mark J Graham, Daniela S Allende, Paolo Parini and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Review
  7. Article
  8. Article
  9. Perilipins at a glance.Journal of cell science · 2022
    Article
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  11. Article
  12. Article
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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

11 authors at 4 institutions in 2 countries.

Daniel FergusonDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH.
Jun ZhangDepartment of Pathology, Wake Forest School of Medicine, Winston-Salem, NC.
Matthew A DavisDepartment of Pathology, Wake Forest School of Medicine, Winston-Salem, NC.
Robert N HelsleyDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH.
Lise-Lotte VedinClinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
Richard G LeeClinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
Rosanne M CrookeClinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
Mark J GrahamClinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
Daniela S AllendeDepartment of Anatomic Pathology, Cleveland Clinic, Cleveland, OH.
Paolo PariniClinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
J Mark BrownDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH brownm5@ccf.org.
Karolinska Institutet · SEWake Forest University · USCleveland Clinic Lerner College of Medicine · USCleveland Clinic · US

Funding

Project Two - Exercise Training Decreases Alcohol Drinking by an FGF21-Dependent MechanismP50AA024333 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI Thomas M McIntyre · 2016 to 2026
$19.6M
TRAINING PROGRAM IN IMMUNOLOGY AND PATHOGENESIST32AI007401 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Martha Ann Alexander-Miller · 1991 to 2026
$4.4M
Enzymatic Control of Trimethylamineoxide (TMAO)Induced AtherosclerosisR01HL122283 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI BROWN, JONATHAN MARK · 2014 to 2018
$2.0M
Mechanisms Regulating Non-biliary Fecal Sterol LossR00HL096166 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BROWN, JONATHAN MARK · 2011 to 2013
$733k
NHLBI NIH HHS R00 HL096166NHLBI NIH HHS R01 HL122283NIAAA NIH HHS P50 AA024333NIAID NIH HHS T32 AI007401
6 · The paper itself

Abstract

Hepatitis C virus (HCV) is an enveloped RNA virus responsible for 170 million cases of viral hepatitis worldwide. Over 50% of chronically infected HCV patients develop hepatic steatosis, and steatosis can be induced by expression of HCV core protein (core) alone. Additionally, core must associate with cytoplasmic lipid droplets (LDs) for steatosis development and viral particle assembly. Due to the importance of the LD as a key component of hepatic lipid storage and as a platform for HCV particle assembly, it seems this dynamic subcellular organelle is a gatekeeper in the pathogenesis of viral hepatitis. Here, we hypothesized that core requires the host LD scaffold protein, perilipin (PLIN)3, to induce hepatic steatosis. To test our hypothesis in vivo, we have studied core-induced hepatic steatosis in the absence or presence of antisense oligonucleotide-mediated knockdown of PLIN3. PLIN3 knockdown blunted HCV core-induced steatosis in transgenic mice fed either chow or a moderate fat diet. Collectively, our studies demonstrate that the LD scaffold protein, PLIN3, is essential for HCV core-induced hepatic steatosis and provide new insights into the pathogenesis of HCV.

Indexed as

AnimalsFatty LiverGene Knockdown TechniquesGenotypeHepacivirusHepatitis CHumansLipid DropletsLipid MetabolismLiverMiceOligonucleotides, AntisensePerilipin-3Oligonucleotides, AntisensePerilipin-3lipid dropletslipoproteins/metabolismlivertriglyceride

Identifiers

PMID27941027
PMCPMC5282958
OpenAlexW2560289760

What OpenQuestion holds

Textmetadata
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.