Evidence map›Paper›PMID 32267915›Full record

ArticleThe Journal of experimental medicine2020

Hepatic stellate cell-specific knockout of transcriptional intermediary factor 1γ aggravates liver fibrosis.

Eun Ju Lee, Injoo Hwang, Ji Yeon Lee, Jong Nam Park, Keun Cheon Kim, Irene Kim, Dodam Moon, Hyomin Park, Seo-Yeon Lee, Hong Sug Kim and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. [Advances of TRIM superfamily proteins in chronic liver disease and hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Vitamin A: too good to be bad?Frontiers in pharmacology · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Novel Therapeutic Targets in Liver Fibrosis.Frontiers in molecular biosciences · 2021
    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

13 authors at 3 institutions in 1 country.

Eun Ju LeeBiomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
Injoo HwangMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Ji Yeon LeeMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Jong Nam ParkMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Keun Cheon KimMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Irene KimMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Dodam MoonMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Hyomin ParkMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Seo-Yeon LeeBiomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
Hong Sug KimDivision of Genome Application, Macrogen, Inc., Seoul, Republic of Korea.
Dae Won JunDepartment of Internal Medicine, Hanyang University School of Medicine, Seoul, Republic of Korea.
Sung-Hye ParkDepartment of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Hyo-Soo KimMolecular Medicine & Biopharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Seoul National University · KRSeoul National University Hospital · KRHanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor β (TGFβ) is a crucial factor in fibrosis, and transcriptional intermediary factor 1γ (TIF1γ) is a negative regulator of the TGFβ pathway; however, its role in liver fibrosis is unknown. In this study, mesenchymal stem cells derived from human embryonic stem cells (hE-MSCs) that secrete hepatocyte growth factor (HGF) were used to observe the repair of thioacetamide (TAA)-induced liver fibrosis. Our results showed that TIF1γ was significantly decreased in LX2 cells when exposed to TGFβ1. Such decrease of TIF1γ was significantly prevented by co-culture with hE-MSCs. Interaction of TIF1γ with SMAD2/3 and binding to the promoter of the α-smooth muscle gene (αSMA) suppressed αSMA expression. Phosphorylation of cAMP response element-binding protein (CREB) and binding on the TIF1γ promoter region induced TIF1γ expression. Furthermore, hepatic stellate cell-specific TIF1γ-knockout mice showed aggravation of liver fibrosis. In conclusion, loss of TIF1γ aggravates fibrosis, suggesting that a strategy to maintain TIF1γ during liver injury would be a promising therapeutic approach to prevent or reverse liver fibrosis.

Indexed as

ActinsAnimalsCells, CulturedCyclic AMP Response Element-Binding ProteinHepatic Stellate CellsHepatocyte Growth FactorHumansLiver CirrhosisMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMice, KnockoutMice, NudeMice, TransgenicPhosphorylationPromoter Regions, GeneticACTA2 protein, humanActinsCyclic AMP Response Element-Binding ProteinHepatocyte Growth FactorSmad ProteinsThioacetamideTranscription FactorsTRIM33 protein, humanTrim33 protein, mouse

Identifiers

PMID32267915
PMCPMC7971140
OpenAlexW3014943398

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.