Evidence map›Paper›PMID 29701903›Full record

ArticleMolecular nutrition & food research2018

Impact of miR-140 Deficiency on Non-Alcoholic Fatty Liver Disease.

Benjamin Wolfson, Pang-Kuo Lo, Yuan Yao, Linhao Li, Hongbing Wang, Qun Zhou

Open access · greenAbstract read
In one paragraph

Article in Molecular nutrition & food research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. NUDT7 Loss PromotesCancers · 2020
    Article
  6. 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

6 authors at 1 institution in 1 country.

Benjamin WolfsonDepartment of Biochemistry and Molecular Biology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, 21201, USA.
Pang-Kuo LoDepartment of Biochemistry and Molecular Biology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, 21201, USA.
Yuan YaoDepartment of Biochemistry and Molecular Biology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, 21201, USA.
Linhao LiDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD, 21202, USA.
Hongbing WangDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD, 21202, USA.
Qun ZhouDepartment of Biochemistry and Molecular Biology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, 21201, USA.
University of Maryland, Baltimore · US

Funding

miR-140 and Breast Cancer PreventionR01CA163820 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHOU, QUN · 2012 to 2016
$1.6M
Shikonin and Nrf2 ChemopreventionR01CA157779 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHOU, QUN · 2013 to 2017
$1.4M
Function and Regulation of SLC13A5 in the LiverR01GM121550 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI WANG, HONGBING · 2018 to 2021
$1.3M
NCI NIH HHS R01 CA157779NCI NIH HHS R01 CA163820NIGMS NIH HHS R01 GM121550
6 · The paper itself

Abstract

scopeWe have previously shown that loss of miR-140 has a pro-fibrotic effect in the mammary gland. This study aims to investigate whether miR-140 loss and obesity act synergistically to promote non-alcoholic fatty liver disease (NAFLD), and to identify the underlying mechanisms. METHODS AND

resultsLiver tissues were isolated from lean-fat-diet and high-fat-diet fed wild-type and miR-140 knockout mice. Using molecular staining and immunohistochemistry techniques, increased development of NAFLD and fibrotic indicators in miR-140 knockout mice were identified. Utilizing an in vitro model system, miR-140 was demonstrated to target TLR-4, and miR-140 overexpression was shown to be sufficient to inhibit palmitic acid signaling through the TLR-4/NFκB pathway.

conclusionThese findings demonstrate that loss of miR-140 results in increased expression of TLR-4, sensitizing cells to palmitic acid signaling and in increased inflammatory activity through the TLR4/NFκB pathway. This signaling axis promotes NAFLD development in a high-fat diet context and indicates the potential utility of miR-140 rescue as a therapeutic strategy in NAFLD.

Indexed as

AnimalsCells, CulturedCollagenDiet, High-FatFemaleHumansInflammationMiceMice, Inbred C57BLMicroRNAsNF-kappa BNon-alcoholic Fatty Liver DiseaseToll-Like Receptor 4CollagenMicroRNAsMirn140 microRNA, humanMIRN140 microRNA, mouseNF-kappa BToll-Like Receptor 4miR-140non-alcoholic fatty liver disease (NAFLD)obesitypalmitic acidTLR-4

Identifiers

PMID29701903
PMCPMC6280970
OpenAlexW2802217048

What OpenQuestion holds

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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.