ArticleAntioxidants (Basel, Switzerland)2021
Fisetin Inhibits NLRP3 Inflammasome by Suppressing TLR4/MD2-Mediated Mitochondrial ROS Production.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Glycyrrhetinic acid augments lipid catabolism via immune-neural modulation in adipose tissue.Journal of advanced research · 2026Article
- PLGA Nanoparticle-Mediated Sustained Release of Fisetin for Intra-Articular Therapy of Temporomandibular Joint Osteoarthritis.International journal of molecular sciences · 2026Article
- Restricting intracellularAutophagy · 2026Article
- Mechanistic Analysis of Fisetin in Liver Diseases and Its Potential Therapeutic Application in IFALD-A Review of In Vitro and In Vivo Studies.Nutrients · 2025Review
- Fisetin carbon dots alleviate periodontitis by enhancing mitophagy through regulation of sirtuin 3 SUMOylation.Journal of nanobiotechnology · 2025Article
- Role of HSP90 in Type 2 Diabetes Mellitus and Its Association with Liver Diseases.Molecular biotechnology · 2025Review
- The Role of Myeloid Differentiation Factor 2 in Stroke: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Fisetin alleviates oxidative stress and promotes porcine early embryonic development via activation of the NRF2-ARE signalling pathway.Animal bioscience · 2025Article
- Flavonoids regulating NLRP3 inflammasome: a promising approach in alleviating diabetic peripheral neuropathy.Inflammopharmacology · 2025Review
- Anticancer Plant Secondary Metabolites Evicting Linker Histone H1.2 from Chromatin Activate Type I Interferon Signaling.International journal of molecular sciences · 2025Article
- Inflammasomes Are Influenced by Epigenetic and Autophagy Mechanisms in Colorectal Cancer Signaling.International journal of molecular sciences · 2024Review
- 2,4'-Dihydroxybenzophenone: A Promising Anti-Inflammatory Agent Targeting Toll-like Receptor 4/Myeloid Differentiation Factor 2-Mediated Mitochondrial Reactive Oxygen Species Production during Lipopolysaccharide-Induced Systemic Inflammation.ACS pharmacology & translational science · 2024Article
- The Role of Pyroptosis and Autophagy in the Nervous System.Molecular neurobiology · 2024Review
- Gadolinium-Based Magnetic Resonance Theranostic Agent with Gallic Acid as an Anti-Neuroinflammatory and Antioxidant Agent.Antioxidants (Basel, Switzerland) · 2024Article
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- Fast and quantitative mitophagy assessment by flow cytometry using theFrontiers in cell and developmental biology · 2024Article
- Effects of Fisetin Treatment on Cellular Senescence of Various Tissues and Organs of Old Sheep.Antioxidants (Basel, Switzerland) · 2023Article
- Fisetin, a Natural Polyphenol, Ameliorates Endometriosis Modulating Mast Cells Derived NLRP-3 Inflammasome Pathway and Oxidative Stress.International journal of molecular sciences · 2023Article
- HSF1 Alleviates Brain Injury by Inhibiting NLRP3-Induced Pyroptosis in a Sepsis Model.Mediators of inflammation · 2023Article
- Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
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Abstract
Fisetin has numerous therapeutic properties, such as anti-inflammatory, antioxidative, and anticancer effects. However, the mechanism by which fisetin inhibits NLRP3 inflammasome remains unclear. In this study, we observed that fisetin bound to TLR4 and occluded the hydrophobic pocket of MD2, which in turn inhibited the binding of LPS to the TLR4/MD2 complex. This prevented the initiation of scaffold formation by the inhibition of MyD88/IRAK4 and subsequently downregulated the NF-κB signaling pathway. The result also demonstrated that fisetin downregulated the activation of the NLRP3 inflammasome induced by LPS and ATP (LPS/ATP) and the subsequent maturation of IL-1β. Fisetin also activated mitophagy and prevented the accumulation of damaged mitochondria and the excessive production of mitochondrial reactive oxygen species. The transient knockdown of
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