Evidence map›Paper›PMID 30735525›Full record

ArticlePloS one2019

Epidermal growth factor receptor inhibition attenuates non-alcoholic fatty liver disease in diet-induced obese mice.

Sorim Choung, Ji Min Kim, Kyong Hye Joung, Eaum Seok Lee, Hyun Jin Kim, Bon Jeong Ku

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Sexual dimorphism in the liver.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Loss of hepatocyte-specific RECK exacerbates metabolic dysfunction-associated steatohepatitis.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  9. Article
  10. Review
  11. Investigating the Mechanisms ofFood science & nutrition · 2025
    Article
  12. Current and emerging strategies for the prevention of hepatocellular carcinoma.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023
    Review
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.

Sorim ChoungDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon, South Korea.
Ji Min KimDepartment of Internal Medicine, College of Medicine, Chungnam National University School of Medicine, Daejeon, South Korea.
Kyong Hye JoungDepartment of Internal Medicine, College of Medicine, Chungnam National University School of Medicine, Daejeon, South Korea.
Eaum Seok LeeDepartment of Internal Medicine, College of Medicine, Chungnam National University School of Medicine, Daejeon, South Korea.
Hyun Jin KimDepartment of Internal Medicine, College of Medicine, Chungnam National University School of Medicine, Daejeon, South Korea.
Bon Jeong KuDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon, South Korea.ORCID 0000-0002-3414-8949
Chungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the main causes of chronic liver disease. NAFLD begins with excessive lipid accumulation in the liver and progresses to nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is closely linked to dysregulated hepatic lipid metabolism. Although recent studies have reported that epidermal growth factor receptor (EGFR) signaling regulates lipid metabolism, the roles of EGFR and EGFR inhibitors as modulators of lipid metabolism are largely unknown. Here, we investigated whether inhibiting EGFR using the EGFR tyrosine kinase inhibitor (TKI) PD153035 improves NAFLD. Our results demonstrate that EGFR was activated in liver tissues from high fat diet (HFD)-induced NAFLD mice. Inhibiting EGFR using PD153035 significantly reduced phosphatidylinositol-3-kinase/protein kinase B signaling and sterol responsive elementary binding protein 1 and 2 expression, which prevented HFD-induced hepatic steatosis and hypercholesterolemia by reducing de novo lipogenesis and cholesterol synthesis and enhancing fatty acid oxidation. Additionally, inhibiting EGFR improved HFD-induced glucose intolerance. In conclusion, these results indicate that EGFR plays an important role in NAFLD and is a potential therapeutic target.

Indexed as

Diabetes Mellitus, ExperimentalNon-alcoholic Fatty Liver DiseaseAnimalsCell Line, TumorDietary FatsErbB ReceptorsHumansLipogenesisMaleMiceQuinazolinesSignal Transduction4-((3-bromophenyl)amino)-6,7-dimethoxyquinazolineDietary FatsEGFR protein, mouseErbB ReceptorsQuinazolines

Identifiers

PMID30735525
PMCPMC6368280
OpenAlexW2914219472

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.