ArticleBiochemistry and biophysics reports2026
Limited impact of NLRP3 inflammasome deficiency on diet-induced metabolic dysfunction-associated steatohepatitis in mice.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD) and a growing cause of chronic liver disease worldwide. Although the NLRP3 inflammasome has been implicated in MASH pathogenesis, its contribution remains controversial across experimental models. We investigated whether systemic deletion of NLRP3 attenuates diet-induced MASH using a choline-deficient, l-amino acid-defined, high-fat diet (CDAHFD) model. Wild-type (WT) and NLRP3-knockout (KO) mice were fed either CDAHFD or a control diet. CDAHFD induced comparable hepatic steatosis, inflammation, fibrosis, and serum alanine aminotransferase elevation in both genotypes. Systemic and hepatic oxidative stress was also comparable between WT and NLRP3-KO mice. Total NAFLD activity scores did not differ between the two genotypes. Although hepatic
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