ArticleJournal of lipid research2023
Genetic deletion or pharmacologic inhibition of the Nlrp3 inflammasome did not ameliorate experimental NASH.
Article in Journal of lipid research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Limited impact of NLRP3 inflammasome deficiency on diet-induced metabolic dysfunction-associated steatohepatitis in mice.Biochemistry and biophysics reports · 2026Article
- Article
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- Inhibition of the NLRP3 Inflammasome With MCC950 Improves Gut Health in Huntington's Disease Mice.Journal of neurochemistry · 2026Article
- β-sitosterol attenuates hepatic lipid accumulation and fibrosis via NLRP3 signaling in MASH mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Beyond cardiovascular protection: a conceptual and translational review of the hepato-specific mechanisms of statins in metabolic dysfunction-associated steatotic liver disease (MASLD).Frontiers in pharmacology · 2026Review
- MASH: the nexus of metabolism, inflammation, and fibrosis.The Journal of clinical investigation · 2025Review
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- NLRP3 and beyond: inflammasomes as central cellular hub and emerging therapeutic target in inflammation and disease.Frontiers in immunology · 2025Review
- Innate Immunity and MASLD.Biomolecules · 2024Review
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
It has been postulated that inflammasomes, in particular the NLRP3 (NLR family pyrin domain containing 3) inflammasome, mediate the necroinflammation and fibrosis that characterize nonalcoholic steatohepatitis (NASH) by engaging innate immune responses. We aimed to investigate the impact of genetic deletion or pharmacologic inhibition of the NLRP3 inflammasome on experimental steatohepatitis. Global Nlrp3 KO (expected to inhibit the NLRP3 inflammasome) or Casp1 KO (expected to inhibit all inflammasomes) mice were compared to wild type controls after 6 months on a high-fat, high-cholesterol (HFHC, 1% cholesterol) diet known to induce fibrosing steatohepatitis. Additionally, wildtype mice on a HFHC diet (0.75% or 0.5% cholesterol) for 6 months were either treated or not treated with an oral, pharmacologic inhibitor of Nlrp3 (MCC950) that was delivered in the drinking water (0.3 mg/ml). We found that genetic deletion or pharmacologic inhibition of the NLRP3 inflammasome did not ameliorate any of the histological components of fibrosing NASH in HFHC-fed mice. Collectively, these results do not support NLRP3 inhibition as a potential target for human NASH.
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Registered trials
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