ReviewHepatology communications2026
Hepatocyte-hepatic stellate cell interactions in liver fibrosis: Mechanisms and therapeutic implications.
Review in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- Size-Dependent Differences in the Effects of Low-Dose Selenium Nanoparticles on Chronic Thioacetamide Toxicosis Accompanying HCC Progression in Mice.Biological trace element research · 2026Article
- Development of a matrix-supported 2.5-dimensional co-culture model: anRSC advances · 2026Article
- Hexokinase-3 upregulation and histone H3K18 lactylation mediate murine liver fibrosis induced by Echinococcus multilocularis.PLoS neglected tropical diseases · 2026Article
- Therapeutic Potential of Cytoglobin and Neuroglobin in Oxidative Stress-Driven Liver Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Cognitive-Enhancing Effects of Bioactive Compounds and Traditional Herbal Medicines in Elderly Patients with Metabolic Syndrome.Biomolecules · 2026Review
- The role of tryptophan-AhR signaling in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD): implications for therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic fibrosis, driven by chronic liver injury, results from complex interactions between hepatocytes and hepatic stellate cells (HSCs). In response to hepatocyte damage, activated HSCs undergo transdifferentiation into myofibroblast-like cells, contributing to the accumulation of extracellular matrix (ECM) components and the progression of fibrosis. This review explores the intricate bidirectional crosstalk between hepatocytes and HSCs, focusing on the molecular mechanisms underlying their interactions during liver fibrosis. Hepatocytes, upon injury, release inflammatory mediators, reactive oxygen species (ROS), and exosomes, which activate HSCs and promote fibrotic progression. Conversely, activated HSCs exacerbate hepatocyte dysfunction through cytokine release, ECM remodeling, and mechanical stress. Key signaling pathways, including transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), and oxidative stress mechanisms, are central to these processes. The review also discusses current challenges in targeting hepatic fibrosis and proposes future research directions, including the use of multi-omics technologies to unravel the dynamic spatiotemporal interactions between hepatocytes and HSCs. Understanding this intricate regulatory network will be crucial for the development of novel therapeutic strategies to reverse liver fibrosis and improve patient outcomes.
Indexed as
Identifiers
What Socratic 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 Socratic graph.