ArticleCell reports. Medicine2025
Treatment of IL-18-binding protein biologics suppresses fibrotic progression in metabolic dysfunction-associated steatohepatitis.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- MASLD: Spatial Mechanisms and New Therapeutics.Biomolecules · 2026Review
- Reconsidering the role of IL-18BP in MASH: methodological perspectives and clarification of prior findings.Hepatology international · 2026Article
- Dietary oils modulate inflammatory and oxidative responses in pigs: Associations with hepatic gene expression.Veterinary and animal science · 2026Article
- TPM-like manipulations exerted an antidepressant effect and regulated amino acid metabolism and GHR/IGF-1 pathway in the liver in adolescent female CUMS rats.Frontiers in physiology · 2026Article
- Interleukin-18 in obesity and obesity-related metabolic diseases.Nature reviews. Endocrinology · 2026Article
- PYHIN proteins: guardians or contributors to hepatitis B virus pathogenesis?Frontiers in immunology · 2026Review
- He-He-Shu-Yang formula alleviates liver fibrosis by inhibiting hepatic stellate cell activationWorld journal of hepatology · 2025Article
- Eosinophil recruitment and activation in the central nervous system of patients with subarachnoid neurocysticercosis.Journal of neuroinflammation · 2025Article
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Authors and funding
17 authors.
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Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease characterized by inflammation and fibrosis, with enhanced interleukin-18 (IL-18) signaling. IL-18-binding protein (IL-18BP) neutralizes IL-18, but its therapeutic potential in MASH is unclear. We find elevated IL-18BP and IL-18 levels in patients with MASH and mice, with free IL-18 correlating with disease severity. IL-18 stimulates interferon-gamma (IFNγ) production in CD4 T cells, increasing hepatic IL-18BP. IL-18BP-deficient mice show worsened liver inflammation and fibrosis. We develop a human IL-18BP biologics (APB-R3) and inject it to mice to evaluate its pharmacologic efficacy. APB-R3 significantly improves MASH in reducing fibrosis and inflammation and inhibits hepatic stellate cell activation via the cGMP pathway. This study proposes that abrogation of IL-18 signaling by boosting IL-18BP can strongly inhibit the development of MASH-induced fibrosis, and our engineered IL-18BP biologics can become a promising therapeutic candidate for curing MASH.
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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.