Evidence map›Paper›PMID 30214048›Full record

ArticleScientific reports2018

Histone H3K9 demethylase JMJD2B induces hepatic steatosis through upregulation of PPARγ2.

Ji-Hyun Kim, Dae Young Jung, Arulkumar Nagappan, Myeong Ho Jung

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  7. Histone Modifications in NAFLD: Mechanisms and Potential Therapy.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Histone methylation in pre-cancerous liver diseases and hepatocellular carcinoma: recent overview.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

4 authors at 1 institution in 1 country.

Ji-Hyun KimDivision of Longevity and Biofunctional Medicine & Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongnam, 50612, Republic of Korea.
Dae Young JungDivision of Longevity and Biofunctional Medicine & Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongnam, 50612, Republic of Korea.
Arulkumar NagappanDivision of Longevity and Biofunctional Medicine & Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongnam, 50612, Republic of Korea.
Myeong Ho JungDivision of Longevity and Biofunctional Medicine & Healthy Aging Korean Medical Research Center, School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongnam, 50612, Republic of Korea. jung0603@pusan.ac.kr.
Pusan National University · KR

Funding

National Research Foundation of Korea (NRF) 2015R1D1A1A01060558
6 · The paper itself

Abstract

Understanding the epigenetic mechanisms underlying the progression of hepatic steatosis is important for identifying new therapeutic targets against nonalcoholic fatty liver disease (NAFLD). We investigated the functional role of histone demethylase JMJD2B in the pathologic regulation of hepatic steatosis. JMJD2B expression was markedly increased in HepG2 cells treated with palmitate and oleate or liver X receptor agonist T09013178 and in the liver of high-fat diet (HFD)-induced obese mice. Overexpression of JMJD2B using adenovirus in HepG2 cells stimulated the expression of peroxisome proliferator-activated receptor γ2 (PPARγ2) and its steatosis target genes associated with fatty acid uptake and lipid droplet formation, resulting in increased intracellular triglyceride (TG) accumulation. Conversely, knocking down JMJD2B using siRNA reversed JMJD2B-mediated effects in HepG2 cells. The JMJD2B-dependent upregulation of PPARγ2 was associated with the removal of di- and trimethylation of histone H3 lysine 9 on the promoter of PPARγ2. Furthermore, exogeneous expression of JMJD2B using adenovirus in mice resulted in hepatic steatosis when fed a HFD, which was accompanied with increased expression of hepatic PPARγ2 and its steatosis target genes. Together, our results provide novel insights into the pivotal role of JMJD2B in the development of hepatic steatosis through upregulation of PPARγ2 and steatosis target genes.

Indexed as

AnimalsDiet, High-FatFatty LiverGene Expression RegulationHep G2 CellsHumansJumonji Domain-Containing Histone DemethylasesLiverMiceMice, ObeseNon-alcoholic Fatty Liver DiseaseOleic AcidPalmitic AcidsPPAR gammaTriglyceridesJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanOleic AcidPalmitic AcidsPPAR gammaTriglycerides

Identifiers

PMID30214048
PMCPMC6137221
OpenAlexW2892338388

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.