ReviewGenes & diseases2023
Mechanisms of NLRP3 inflammasome-mediated hepatic stellate cell activation: Therapeutic potential for liver fibrosis.
Review in Genes & diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Nifuroxazide Pretreatment Protects Against Acute CdClAntioxidants (Basel, Switzerland) · 2026Article
- Emerging roles of mitophagy in liver fibrosis: Implications for therapy.Acta pharmacologica Sinica · 2026Review
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- Targeting FAPActa pharmaceutica Sinica. B · 2026Article
- Resveratrol Alleviates Arsenic-Induced Liver Fibrosis in Rats by Correcting SIRT1-Mediated Disorder of Hepatic Bile Acid Metabolism.International journal of molecular sciences · 2026Article
- Silent inflammation: a hidden cause of liver fibrosis.Frontiers in pharmacology · 2026Review
- A Novel NLRP3 Inhibitor AMS-17 Rescues Deficits in Long-Term Potentiation Following Mild Traumatic Brain Injury in Adult C57Bl/6 Mice.Hippocampus · 2026Article
- Targeting inflammatory dysregulation in metabolic dysfunction-associated steatotic liver disease rat model: the preventive and therapeutic effects of acetyl-11-keto-beta-boswellic acid.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- PROM2 exacerbates CCl4-Induced liver fibrosis via NLRP3 inflammasome activation and hepatocyte pyroptosis.Cellular and molecular life sciences : CMLS · 2025Article
- Fungal Polysaccharides as Modulators of Molecular Pathways in Liver Health.Molecules (Basel, Switzerland) · 2025Review
- Calcium-sensing receptor: a potential target for liver health and diseases.Journal of translational medicine · 2025Review
- Alcohol-Induced Oxidative Stress and Gut-Liver-Brain Crosstalk: Expanding the Paradigm from ALD to MetALD.Antioxidants (Basel, Switzerland) · 2025Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review.CNS neuroscience & therapeutics · 2025Review
- Identification of pyroptosis-associated gene to predict fibrosis and reveal immune characterization in non-alcoholic fatty liver disease.Scientific reports · 2025Article
- The antifibrotic effect of Vildagliptin and Diaminodiphenyl Sulfone in murine schistosomiasis mansoni.Scientific reports · 2025Article
- Clusterin deficiency exacerbates cholestatic liver disease through ER stress and NLRP3 inflammasome activation.Cell & bioscience · 2025Article
- NLRP3 inflammasome constrains liver regeneration through impairing MerTK-mediated macrophage efferocytosis.Science advances · 2025Article
- Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair.Frontiers in neuroscience · 2025Review
- Metabolism of hepatic stellate cells in chronic liver diseases: emerging molecular and therapeutic interventions.Theranostics · 2025Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The liver injury leads to an inflammatory response, which causes the activation of hepatic stellate cells (HSCs) that further secrete ECM proteins and play an important role in liver fibrosis. Moreover, the inflammatory response is a driving force for fibrogenesis, which is triggered by many types of injuries. Exaggerated inflammatory immune responses are mediated by cytoplasmic protein complexes known as inflammasomes, which are involved in many chronic liver diseases. Inflammasomes are pattern recognition receptors (PRRs) that can sense any microbial motifs known as pathogen-associated molecular patterns (PAMPs), and host- or environmental-derived stress signals known as damage-associated molecular patterns (DAMPs). The inflammasomes cause caspase-mediated proteolytic cleavage of pro-IL-1β and pro-IL-18 into active IL-1β and IL-18. In this review, we provide a comprehensive summary of the important roles of NLRP3 inflammasome in the pathogenesis of liver fibrosis with an emphasis on several direct and indirect pathways responsible for the NLRP3 inflammasome-mediated HSCs activation and fibrogenesis. In addition, we discuss the general pharmacological and genetics strategies for the inhibition of NLRP3 inflammasome activation and its downstream signaling with examples of emerging pharmacotherapeutics, targeting the NLRP3 inflammasome signaling as well as a possible way to develop effective and safer NLRP3 inflammasome inhibitors.
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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.