ReviewWorld journal of gastroenterology2014
Cellular and molecular mechanisms in the pathogenesis of liver fibrosis: An update.
Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
186 citing papers in PubMed, 2 syntheses or guidelines pooled it, 368 citations in OpenAlex.
- A systematic review of the anti-inflammatory and anti-fibrotic potential of human umbilical cord mesenchymal stem cells-derived exosomes in experimental models of liver regeneration.Molecular biology reports · 2024Pooled it
- Efficacy and Safety of Emricasan in Liver Cirrhosis and/or Fibrosis.Clinics (Sao Paulo, Brazil)Pooled it
- Safety, tolerability, pharmacokinetics, and pharmacodynamics of BI 685509, a soluble guanylyl cyclase activator, in healthy volunteers: Results from two randomized controlled trials.Naunyn-Schmiedeberg's archives of pharmacology · 2024Trial
- Tolerability and Pharmacokinetics of Hydronidone, an Antifibrotic Agent for Hepatic Fibrosis, after Single and Multiple Doses in Healthy Subjects: an Open-Label, Randomized, Dose-Escalating, First-in-Human Study.European journal of drug metabolism and pharmacokinetics · 2017Trial
- Results of Multicenter Phase II Study With Imatinib Mesylate in Allogeneic Recipients With Steroid-Refractory Chronic GVHD.Cell transplantationTrial
- Article
- Article
- P7C3 alleviates hepatic fibrosis via targeting eIF4A1-mediated protein translation and autophagy in hepatic stellate cells.Archives of pharmacal research · 2026Article
- Hepatocyte-hepatic stellate cell interactions in liver fibrosis: Mechanisms and therapeutic implications.Hepatology communications · 2026Review
- Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026Review
- Emerging Biomarkers for Early Detection and Prognosis of Liver Diseases.Current pharmaceutical design · 2026Review
- AKF-PD alleviated liver fibrosis by inducing hepatic stellate cell ferroptosis via the HIF-1α/SLC7A11 pathway.European journal of medical research · 2025Article
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- A Proanthocyanidins-Rich Cili (Nutrients · 2025Article
- Article
- Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation.Exploration (Beijing, China) · 2025Article
- Vitamin A toxicity and hepatic pathology: A comprehensive review.World journal of hepatology · 2025Review
- Identification and validation of the fibrosis-related molecular subtypes of hepatocellular carcinoma by bioinformatics.Discover oncology · 2025Article
- Innovative Strategies in the Diagnosis and Treatment of Liver Cirrhosis and Associated Syndromes.Life (Basel, Switzerland) · 2025Review
- Article
126 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There have been considerable recent advances towards a better understanding of the complex cellular and molecular network underlying liver fibrogenesis. Recent data indicate that the termination of fibrogenic processes and the restoration of deficient fibrolytic pathways may allow the reversal of advanced fibrosis and even cirrhosis. Therefore, efforts have been made to better clarify the cellular and molecular mechanisms that are involved in liver fibrosis. Activation of hepatic stellate cells (HSCs) remains a central event in fibrosis, complemented by other sources of matrix-producing cells, including portal fibroblasts, fibrocytes and bone marrow-derived myofibroblasts. These cells converge in a complex interaction with neighboring cells to provoke scarring in response to persistent injury. Defining the interaction of different cell types, revealing the effects of cytokines on these cells and characterizing the regulatory mechanisms that control gene expression in activated HSCs will enable the discovery of new therapeutic targets. Moreover, the characterization of different pathways associated with different etiologies aid in the development of disease-specific therapies. This article outlines recent advances regarding the cellular and molecular mechanisms involved in liver fibrosis that may be translated into future therapies. The pathogenesis of liver fibrosis associated with alcoholic liver disease, non-alcoholic fatty liver disease and viral hepatitis are also discussed to emphasize the various mechanisms involved in liver fibrosis.
Indexed as
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What OpenQuestion holds
Registered trials
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.