ArticlePloS one2023
Lobeglitazone inhibits LPS-induced NLRP3 inflammasome activation and inflammation in the liver.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Deciphering cytochrome P450 reductase role in MASLD: molecular mechanisms and pathophysiological implications.Nature reviews. Gastroenterology & hepatology · 2026Review
- 3-carbamoyl proxyl nitroxide attenuates CClScientific reports · 2026Article
- Host-gut microbiota interactions in health and disease: mechanisms and intervention strategies.Frontiers in microbiology · 2026Review
- Cross-talk between NLRP3 and AIM2 inflammasomes in macrophage activation by LPS and titanium ions.Molecular medicine (Cambridge, Mass.) · 2025Article
- Clusterin inhibits lipopolysaccharide induced liver injury.Scientific reports · 2025Article
- Polysaccharide of Atractylodes macrocephala Koidz alleviate LPS-induced inflammatory liver injury by reducing pyroptosis of macrophage via regulating LncRNA GAS5/miR-223-3p/NLRP3 axis.Frontiers in pharmacology · 2025Article
- Decoding the heterogeneity of liver-resident macrophages in chronic liver diseases: therapeutic responses to immunomodulatory strategies.Frontiers in pharmacology · 2025Review
- Review on the role of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway in diabetes: mechanistic insights and therapeutic implications.Inflammopharmacology · 2024Review
- Mitochondrial Dysfunction in Metabolic Dysfunction Fatty Liver Disease (MAFLD).International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver inflammation is a common feature of chronic liver disease and is often associated with increased exposure of the liver to lipopolysaccharide (LPS). Kupffer cells (KCs) are macrophages in the liver and produce various cytokines. Activation of KCs through the NLRP3 inflammasome pathway leads to release of proinflammatory cytokines and induces hepatocyte injury and hepatic stellate cell (HSC) activation. Lobeglitazone is a peroxisome proliferator-activated receptor gamma ligand and a type of thiazolidinedione that elicits anti-inflammatory effects. However, there is no clear evidence that it has direct anti-inflammatory effects in the liver. This study showed that lobeglitazone reduces LPS-induced NLPR3 inflammasome activation and production of proinflammatory cytokines in primary KCs and hepatocytes. Cytokines secreted by activated KCs increased hepatocyte inflammation and HSC activation, and lobeglitazone inhibited these responses. In addition, lobeglitazone suppressed liver fibrosis by inhibiting LPS-induced transforming growth factor (TGF)-β secretion and TGF-β-induced CTGF expression. The inhibitory effect of lobeglitazone on inflammasome activation was associated with suppression of liver fibrosis. These results suggest that lobeglitazone may be a treatment option for inflammation and fibrosis in the liver.
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