Evidence map›Paper›PMID 33317250›Full record

ReviewClinical and molecular hepatology2021

Anti-fibrotic treatments for chronic liver diseases: The present and the future.

Naoshi Odagiri, Tsutomu Matsubara, Misako Sato-Matsubara, Hideki Fujii, Masaru Enomoto, Norifumi Kawada

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and molecular hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. SNX3 exacerbates hepatic fibrosis by amplifying TGF-Acta pharmaceutica Sinica. B · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Hepatoprotective effect of hUC-MSC secretome in LPS-induced HepG2 cells.Iranian journal of basic medical sciences · 2026
    Article
  8. Article
  9. Sublingual Dripping Pill Formulation ofCurrent issues in molecular biology · 2025
    Article
  10. [Research progress on the mechanistic role and constituents of hepatic macrophages during the occurrence and development of hepatic fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review
  11. Challenges ofFrontiers in cell and developmental biology · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Current investigations for liver fibrosis treatment: between repurposing the FDA-approved drugs and the other emerging approaches.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 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.

Naoshi OdagiriDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Tsutomu MatsubaraDepartment of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Misako Sato-MatsubaraDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Hideki FujiiDepartment of Premier Preventive Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Masaru EnomotoDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Norifumi KawadaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Osaka City University · JP

Funding

Japan Agency for Medical Research and DevelopmentJapan Society for the Promotion of Science J192640002
6 · The paper itself

Abstract

Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

Indexed as

Liver CirrhosisEndothelial CellsHepatic Stellate CellsHumansHypertension, PortalLiverDrug therapyExtracellular matrixFibrosisHepatic stellate cellsMyofibroblasts

Identifiers

PMID33317250
PMCPMC8273638
OpenAlexW3112047391

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.