ReviewThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2025
Liver Fibrosis: Interactions Between Cells and Microenvironments.
Review in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Association of the Stress Hyperglycemia Ratio with Advanced Liver Fibrosis and Mortality in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease: An Analysis of NHANES.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Association of Systemic Inflammatory Indices with Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Metabolic reprogramming in hepatic stellate cells: unveiling a novel therapeutic target for liver fibrosis.Frontiers in physiology · 2026Review
- Exposure-shaped immunometabolic networks in chronic liver disease: translating multi-omics and artificial intelligence into preventive biomarkers.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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a key intermediate stage in the progression of chronic liver disease to end-stage liver cirrhosis. Mortality rises exponentially once it reaches decompensated liver disease. In a healthy liver microenvironment, hepatocytes, Kupffer cells, hepatic stellate cells (HSCs), liver sinusoidal endothelial cells, and other cells interact with extracellular matrix (ECM) to maintain cell stability and liver function. Different types of liver injury (such as viral hepatitis and alcoholic liver injury) can cause liver fibrosis. Liver injury signals activate Kupffer cells and recruit immune cells, leading to liver inflammation. This inflammation, together with liver injury, stimulates the activation of HSCs. Activated HSCs migrate to injury sites and secrete ECM. The ECM increase and stiffening contribute to fibrosis. Microenvironment changes alter cell phenotypes, perpetuating HSC activation. This article explores liver fibrosis mechanisms, reviews cellular and microenvironmental changes, summarizes fibrosis characteristics, and provides insights for clinical treatment.
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.