ReviewGastroenterology2025
Regulation of Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis.
Review in Gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed.
- Review
- Hijacking Host Communication: The Central Role of Extracellular Vesicles in Infectious Disease Pathogenesis.Cells · 2026Review
- From Single Agents to Synergy: Redefining Therapeutic Strategies in MASLD.International journal of molecular sciences · 2026Review
- MRI-derived visceral adipose tissue quantification enhances stratification of nonalcoholic steatohepatitis severity and fibrosis in obesity.Abdominal radiology (New York) · 2026Article
- ABCC6 in Cellular Metabolic Homeostasis: Biochemical Links to Extracellular Nucleotide Signaling, Mitochondrial Stress, and Senescence.Cell biochemistry and biophysics · 2026Review
- Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Review
- Gut Microbiota, Immunity, and Metabolism in the Progression From Chronic Liver Disease to Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- p21-activated kinase 4 drives hepatic stellate cell activation and liver fibrosis through the phosphorylation of YAP at T428.Signal transduction and targeted therapy · 2026Article
- Review
- 6-Gingerol alleviates hepatic fibrosis via inhibiting glycolytic reprogramming by targeting IGF2BP2.Chinese herbal medicines · 2026Article
- Therapeutic targeting of AREL1 in hepatic stellate cells attenuates MASH-related liver fibrosis.Nature communications · 2026Article
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Reduction in Hepatic Phosphatidylcholine Biosynthesis Promotes MASH Through Copper Deficiency.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- Review
- A Novel Anti-Fibrotic Role of G-Protein-Coupled Receptor 119 in Hepatic Stellate Cells.Biomolecules & therapeutics · 2026Article
- THEMIS attenuates MASH by suppressing disease-associated hepatocyte induction and hepatocyte senescence in mice.The Journal of clinical investigation · 2026Article
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
Abstract
Hepatic stellate cells (HSCs) play a crucial role in the pathogenesis of liver fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), a condition characterized by excessive fat accumulation in the hepatocytes, unrelated to alcohol consumption. In a healthy liver, HSCs are quiescent, store vitamin A, and function as pericytes. However, in response to liver injury and inflammation, HSCs become activated. In MASH, HSC activation is driven by metabolic stress, lipotoxicity, and chronic inflammation. Injured hepatocytes, recruited macrophage, capillarized sinusoidal endothelial cells, and permeable intestinal epithelium may each contribute to activating HSCS. This leads to a unique inflammatory environment that promotes fibrosis. MASH HSCs change their metabolism to favor glycolysis, glutaminolysis, and lactate generation. Activated HSCs transform into myofibroblast-like cells, producing excessive extracellular matrix components that result in fibrosis. In addition, HSCs in MASH have inflammatory and intermediate activated phenotypes. This fibrotic process is a key feature of MASH, which can lead to cirrhosis and liver cancer. Understanding the mechanisms of HSC activation and their role in MASH progression is essential for developing targeted therapies to treat and prevent liver fibrosis in affected individuals.
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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.