ReviewWorld journal of clinical cases2022
Pathophysiological mechanisms of hepatic stellate cells activation in liver fibrosis.
Review in World journal of clinical cases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Effect of nano-curcumin supplementation on liver fibrosis in patients with NAFLD-associated fibrosis: a double-blind randomized controlled trial.Scientific reports · 2025Trial
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Effect of Short-Chain Fatty Acids In Vivo on the Treatment of CCLBiomedicines · 2026Article
- Prevalence and biomarker profiles of HBV/HDV coinfection and occult HBV infection among patients attending Bimbilla Hospital, Northern Ghana.BMC infectious diseases · 2026Article
- Pancreatic Cancer-Derived Small Extracellular Vesicles Remodel Hepatic Pre-Metastatic Niche via Hybrid Epithelial-Mesenchymal States.International journal of molecular sciences · 2026Article
- Retinol-guided liposomal platform for targeted pirfenidone delivery in hepatic fibrosis.Journal of nanobiotechnology · 2026Article
- Therapeutic Potential of Cytoglobin and Neuroglobin in Oxidative Stress-Driven Liver Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Peptide-Functionalized Liposomal Nanocarriers for Targeted Therapy of Liver Fibrosis and Hepatocellular Carcinoma: Design, Mechanisms, and Clinical Prospects.ACS pharmacology & translational science · 2026Review
- Review
- The role and mechanisms of vitamin A in suppressing hepatic stellate cell activation.Apoptosis : an international journal on programmed cell death · 2026Article
- Single-cell profiling reveals lineage-specific fibroblast stromal subtypes drive ECM remodeling and immune modulation in the hepatocellular carcinoma tumor microenvironment.Medical oncology (Northwood, London, England) · 2026Article
- Multi-Target Intervention of Traditional Chinese Medicine in Metabolic Dysfunction-Associated Steatohepatitis: Comprehensive Treatment Strategies from Lipotoxicity to Immune Regulation.International journal of general medicine · 2026Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
- Identification of Key Targets of Herbal Compounds for Liver Fibrosis Using Network Pharmacology Combined With Transcriptomics.Gastroenterology research and practice · 2026Article
- Bisphenol F and Steatotic Liver Disease: Resolving the PXR Paradox Through Stress Pathway Mechanisms.Biomedicines · 2025Review
- The Diagnostic Potential and Regulatory Mechanisms of miR-3180-3p in Metabolic Dysfunction-Associated Fatty Liver Disease with Respect to Inflammation and Oxidative Stress.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Identifying SUMOylation-related genes in liver fibrosis with bioinformatics and experimental models for diagnostic insights.Scientific reports · 2025Article
- Alcohol-Induced Oxidative Stress and Gut-Liver-Brain Crosstalk: Expanding the Paradigm from ALD to MetALD.Antioxidants (Basel, Switzerland) · 2025Review
- The Influence of Irisin on Selected Organs-The Liver, Kidneys, and Lungs: The Role of Physical Exercise.Cells · 2025Review
- Reprogramming cellular senescence of hepatic stellate cells to combat liver fibrosis by targeted nanodrugs.Materials today. Bio · 2025Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Liver fibrosis is a complex pathological process controlled by a variety of cells, mediators and signaling pathways. Hepatic stellate cells play a central role in the development of liver fibrosis. In chronic liver disease, hepatic stellate cells undergo dramatic phenotypic activation and acquire fibrogenic properties. This review focuses on the pathophysiological mechanisms of hepatic stellate cells activation in liver fibrosis. They enter the cell cycle under the influence of various triggers. The "Initiation" phase of hepatic stellate cells activation overlaps and continues with the "Perpetuation" phase, which is characterized by a pronounced inflammatory and fibrogenic reaction. This is followed by a resolution phase if the injury subsides. Knowledge of these pathophysiological mechanisms paved the way for drugs aimed at preventing the development and progression of liver fibrosis. In this respect, impairments in intracellular signaling, epigenetic changes and cellular stress response can be the targets of therapy where the goal is to deactivate hepatic stellate cells. Potential antifibrotic therapy may focus on inducing hepatic stellate cells to return to an inactive state through cellular aging, apoptosis, and/or clearance by immune cells, and serve as potential antifibrotic therapy. It is especially important to prevent the formation of liver cirrhosis since the only radical approach to its treatment is liver transplantation which can be performed in only a limited number of countries.
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