ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Interleukin-1 participates in the progression from liver injury to fibrosis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 2 of them syntheses that pooled it.
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Who cites it
144 citing papers in PubMed, 2 syntheses or guidelines pooled it, 275 citations in OpenAlex.
- A Chinese case series of Schnitzler syndrome and complete remission in one tocilizumab-treated patient.Clinical rheumatology · 2020Pooled it
- Transforming growth factor-β genetic polymorphisms on development of liver cirrhosis in a meta-analysis.Molecular biology reports · 2013Pooled it
- Autologous macrophage therapy for liver cirrhosis: a phase 2 open-label randomized controlled trial.Nature medicine · 2025Trial
- A human single-cell atlas identifies OLR1Nature genetics · 2026Article
- Interleukin-1α Mediates Pancreatic Fibroblast Activation, Regulates Immune Cell Recruitment and Fibrosis in Acute and Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Apple Seed Extract Post-Treatment Alters Selected IGF-Related and Extracellular Matrix-Associated Markers Following Tobacco Leaf Extract-Induced Histological Liver Injury.International journal of molecular sciences · 2026Article
- Article
- Diacerein improves liver fibrosis, steatosis, and atherosclerosis in ApoE knockout mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways.Diseases (Basel, Switzerland) · 2026Review
- Microplastics in metabolic dysfunction-associated steatotic liver disease: An emerging threat to liver health.World journal of hepatology · 2025Review
- The Intriguing Roles of Cytokines in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Narrative Review.Current obesity reports · 2025Review
- IL-1b-Bearing NETs: Bridging Inflammation to Early Cirrhosis in Hepatitis B.International journal of molecular sciences · 2025Article
- p-Cymene inhibits pro-fibrotic and inflammatory mediators to prevent hepatic dysfunction.Open life sciences · 2025Article
- Regulation of hepatic Sirt1 expression and lipid metabolism through TNF receptor signaling.Frontiers in immunology · 2025Article
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
- The role of the interleukin family in liver fibrosis.Frontiers in immunology · 2025Review
- Linking Antibodies Against Apolipoprotein A-1 to Metabolic Dysfunction-Associated Steatohepatitis in Mice.International journal of molecular sciences · 2024Article
- Evaluating the antifibrotic potential of naringenin, asiatic acid, and icariin using murine and human precision-cut liver slices.Physiological reports · 2024Article
- NLRP3 inflammasome inhibition decreasesInfection and immunity · 2024Article
- Combined inhibition of IL-1, IL-33 and IL-36 signalling by targeting IL1RAP ameliorates skin and lung fibrosis in preclinical models of systemic sclerosis.Annals of the rheumatic diseases · 2024Article
84 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin-1 (IL-1) is rapidly expressed in response to tissue damage; however, its role in coordinating the progression from injury to fibrogenesis is not fully understood. Liver fibrosis is a consequence of the activation of hepatic stellate cells (HSCs), which reside within the extracellular matrix (ECM) of subsinusoids. We have hypothesized that, among the hepatic inflammatory cytokines, IL-1 may directly activate HSCs through autocrine signaling and stimulate the matrix metalloproteinases (MMPs) produced by HSCs within the space of Disse, resulting in liver fibrogenesis. In this study, we first established a temporal relationship between IL-1, MMPs, HSC activation, and early fibrosis. The roles of IL-1 and MMP-9 in HSC activation and fibrogenesis were determined by mice deficient of these genes. After liver injury, IL-1, MMP-9, and MMP-13 levels were found to be elevated before the onset of HSC activation and fibrogenesis. IL-1 receptor-deficient mice exhibited ameliorated liver damage and reduced fibrogenesis. Similarly, advanced fibrosis, as determined by type-I and -III collagen mRNA expression and fibrotic septa, was partially attenuated by the deficiency of IL-1. In the early phase of liver injury, the MMP-9, MMP-13, and TIMP-1 expression correlated well with IL-1 levels. In injured livers, MMP-9 was predominantly colocalized to desmin-positive cells, suggesting that HSCs are MMP-producing cells in vivo. MMP-9-deficient mice were partially protected from liver injury and HSC activation. Thus IL-1 is an important participant, along with other cytokines, and controls the progression from liver injury to fibrogenesis through activation of HSCs in vivo.
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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.