Evidence map›Paper›PMID 26984260›Full record

ArticleScientific reports2016

Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia.

Soo Min Lee, Dara Nguyen, Marie Anand, Ritu Kant, Clemens Köhncke, Ulrike Lisewski, Torsten K Roepke, Zhaoyang Hu, Geoffrey W Abbott

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  7. The KCNE2 potassium channel β subunit is required for normal lung function and resilience to ischemia and reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Article
  9. Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. Article
  11. Article
  12. 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

9 authors at 3 institutions in 3 countries.

Soo Min LeeBioelectricity Laboratory, Dept. of Pharmacology and Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA, USA.
Dara NguyenBioelectricity Laboratory, Dept. of Pharmacology and Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA, USA.
Marie AnandBioelectricity Laboratory, Dept. of Pharmacology and Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA, USA.
Ritu KantBioelectricity Laboratory, Dept. of Pharmacology and Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA, USA.
Clemens KöhnckeExperimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Ulrike LisewskiExperimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Torsten K RoepkeExperimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Zhaoyang HuLaboratory of Anesthesiology &Critical Care Medicine, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Geoffrey W AbbottBioelectricity Laboratory, Dept. of Pharmacology and Dept. of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA, USA.
University of California, Irvine · USMax Delbrück Center · DESichuan University · CN

Funding

K+ channel trafficking and modulation in MinK and MiRP1R01HL079275 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ABBOTT, GEOFFREY W · 2005 to 2015
$4.6M
NHLBI NIH HHS HL079275NHLBI NIH HHS R01 HL079275
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is an increasing health problem worldwide, with genetic, epigenetic, and environmental components. Here, we describe the first example of NAFLD caused by genetic disruption of a mammalian potassium channel subunit. Mice with germline deletion of the KCNE2 potassium channel β subunit exhibited NAFLD as early as postnatal day 7. Using mouse genetics, histology, liver damage assays and transcriptomics we discovered that iron deficiency arising from KCNE2-dependent achlorhydria is a major factor in early-onset NAFLD in Kcne2(─/─) mice, while two other KCNE2-dependent defects did not initiate NAFLD. The findings uncover a novel genetic basis for NAFLD and an unexpected potential factor in human KCNE2-associated cardiovascular pathologies, including atherosclerosis.

Indexed as

Anemia, Iron-DeficiencyAnimalsC-Reactive ProteinDiet, High-FatFemaleGene Regulatory NetworksGerm-Line MutationHomocysteineLiverMaleMiceMice, Inbred C57BLMice, KnockoutNon-alcoholic Fatty Liver DiseasePotassium Channels, Voltage-GatedSequence DeletionC-Reactive ProteinHomocysteineKcne2 protein, mousePotassium Channels, Voltage-GatedTriglycerides

Identifiers

PMID26984260
PMCPMC4794722
OpenAlexW2300513894

What OpenQuestion 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 OpenQuestion graph.