Evidence map›Paper›PMID 29717162›Full record

ArticleScientific reports2018

Growth differentiation factor 15 ameliorates nonalcoholic steatohepatitis and related metabolic disorders in mice.

Kook Hwan Kim, Seong Hun Kim, Dai Hoon Han, Young Suk Jo, Yong-Ho Lee, Myung-Shik Lee

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 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  4. Observational
  5. Review
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  12. GDF-15 Levels in Cirrhosis Are Linked to Hepatic Fibrogenesis, Bacterial Translocation, and Worse Clinical Outcomes.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
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  16. Article
  17. GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025
    Review
  18. Article
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Kook Hwan KimSeverance Biomedical Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea. kookhwankim@gmail.com.
Seong Hun KimDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, 81 Irwon-ro, Gangnam-gu, Seoul, 06351, South Korea.
Dai Hoon HanDepartment of Surgery, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea.
Young Suk JoDepartment of Internal Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea.ORCID 0000-0001-9926-8389
Yong-Ho LeeDepartment of Internal Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea.ORCID 0000-0002-6219-4942
Myung-Shik LeeSeverance Biomedical Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea. mslee0923@yuhs.ac.ORCID 0000-0003-3292-1720
Yonsei University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth differentiation factor 15 (GDF15) is an endocrine hormone belonging to the TGFβ superfamily member. GDF15 administration or GDF15 overexpression has been reported to have anti-obesity and anti-diabetic effects. Although non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) is frequently associated with obesity and insulin resistance, the functional role of endogenous GDF15 and therapeutic effect of GDF15 overexpression in NASH and related metabolic deterioration have not been evaluated. Here, we found that GDF15 expression was increased in the livers of NASH animal models and human subjects with NASH. Elevated expression of GDF15 was due to diet-induced hepatic endoplasmic reticulum (ER) stress. Gdf15-knockout mice exhibited aggravated NASH phenotypes such as increased steatosis, hepatic inflammation, fibrosis, liver injury, and metabolic deterioration. Furthermore, GDF15 directly suppressed expression of fibrosis-related genes and osteopontin (OPN), contributing factors for NASH-related fibrosis, in hepatic stellate cells in vitro and in the liver of mice in vivo. Finally, we found that GDF15-transgenic mice showed attenuation of NASH phenotypes and metabolic deterioration. Therefore, our results suggest that induction of endogenous GDF15 is a compensatory mechanism to protect against the progression of NASH and that GDF15 could be an attractive therapeutic candidate for treatment of NASH and NASH-related metabolic deterioration.

Indexed as

ActinsAnimalsCholine DeficiencyCollagen Type ICollagen Type I, alpha 1 ChainDietDisease Models, AnimalEndoplasmic Reticulum StressGene Expression RegulationGrowth Differentiation Factor 15Hepatic Stellate CellsHumansLiverLiver CirrhosisMaleMethionineActa2 protein, mouseActinsCollagen Type ICollagen Type I, alpha 1 ChainDdit3 protein, mouseGdf15 protein, mouseGrowth Differentiation Factor 15MethionineOsteopontinSpp1 protein, mouseTgfb1 protein, mouseTimp1 protein, mouseTissue Inhibitor of Metalloproteinase-1Transcription Factor CHOPTransforming Growth Factor beta1

Identifiers

PMID29717162
PMCPMC5931608
OpenAlexW2802676890

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.