Inflammasomes in liver fibrosis
Open accessAbstract
Cell death and inflammation are two central elements in the development of liver fibrosis. Inflammasomes are intracellular multiprotein complexes expressed in both hepatocytes and nonparenchymal cells in the liver that are key regulators of inflammation and cell fate. They respond to cellular danger signals by activating caspase 1, releasing the proinflammatory cytokines IL-1β and IL-18, as well as initiating a novel pathway of programmed cell death termed “pyroptosis.” These processes can initiate and perpetuate an abnormal wound-healing response with the principle cellular target being the activation of hepatic stellate cells. From the various inflammasomes, the NLRP3 inflammasome has been increasingly implicated in the pathogenesis of chronic inflammatory liver diseases, including nonalcoholic steatohepatitis, a disease process that is soaring and has evolved as a primary cause of liver fibrosis and need for liver transplantation. In this review, the authors highlight the growing evidence for both indirect and direct effects of inflammasomes in triggering liver fibrosis as well as potential novel targets for antifibrotic therapies.
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The IL-1β receptor antagonist anakinra is currently being evaluated to limit inflammation in patients with alcoholic hepatitis.
“the IL-1β receptor antagonist anakinra is currently being evaluated to limit inflammation in patients with alcoholic hepatitis (126, 127)”
From Immunoregulation of Liver Fibrosis: New Opportunities for Antifibrotic Therapy (2024) · cites this paper as [126]
Hepatocytes secrete inflammatory and fibrogenic cytokines either directly, such as IL-1β and IL-18, or via extracellular vesicles containing CXCL10 and mitochondrial DNA.
“They also secrete inflammatory and fibrogenic cytokines either directly, such as interleukin (IL)-1β and IL-18,35,36 or via extracellular vesicles containing C-X-C motif chemokine ligand (CXCL)10, a ligand for C-X-C motif chemokine receptor (CXCR)3, and mitochondrial DNA, a key TLR9 ligand.37”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [35]
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- Authors
- Alegre, F., Pelegrin, P., & Feldstein, A.
- Affiliations
- Universitat de València (ES)
- Director, Biomedical Research Institute of Murcia (IMIB-Arrixaca), CIBERehd, Clinical University Hospital Virgen de la Arrixaca, Murcia, Spain
- University of California San Diego (US)
- Corresponding author
- Feldstein, Ariel
- Venue
- Seminars in Liver Disease
- Publisher
- Georg Thieme Verlag KG
- Published
- 2017-05
- Volume
- 37
- Issue
- 02
- Pages
- 119-127
- ISSN
- 0272-8087 (ISSN-L)
- 1098-8971
- OpenAlex
- W2619892599
- Cited by
- 176
- References
- 98
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 19 · 2023: 21 · 2022: 31 · 2021: 26 · 2020: 35 · 2019: 18 · 2018: 6 · 2017: 4
- FWCI
- 1.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Seminars in Liver Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (U01AA022489)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK082451)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- inflammasome, liver fibrosis, NLRP3 inflammasome, caspase-1, IL-1β, IL-18, pyroptosis, hepatic stellate cells, nonalcoholic steatohepatitis, chronic liver inflammation, antifibrotic therapy, wound healing
- MeSH terms
- Alarmins, Pyroptosis, NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Anti-Inflammatory Agents, Humans, Liver Cirrhosis, Signal Transduction, Inflammation Mediators, Receptors, Pattern Recognition
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