NLRP3 inhib 
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  • ||||||||||  Journal:  NLRP3-dependent pyroptosis exacerbates Coxsackievirus A16 and Coxsackievirus A10-induced inflammatory response and viral replication in SH-SY5Y cells. (Pubmed Central) -  May 27, 2024   
    Finally, it was further revealed that NLRP3 agonist enhanced the viral replication, but NLRP3 inhibitor suppressed the viral replication, suggesting that NLRP3-driven pyroptosis might support CV-A16 and CV-A10 production in SH-SY5Y cells. Together, our findings demonstrated a mechanism by which CV-A16 and CV-A10 induce inflammatory responses by evoking NLRP3 inflammasome-regulated pyroptosis, which in turn further stimulated the viral replication, providing novel insights into the pathogenesis of CV-A16 and CV-A10 infections.
  • ||||||||||  H2S Improves Skeletal Muscle Insulin Resistance by Inhibiting Pyroptosis via Sirt2 Pathway (Poster Hall (West A4-B2); 1614) -  May 20, 2024 - Abstract #ADA2024ADA_3212;    
    Therefore, we concluded that hydrogen can ameliorate neurological damage and cognitive dysfunction in VaD rats by inhibiting ROS/NLRP3/IL-1?-related oxidative stress and inflammation. H2S regulates skeletal muscle satellite cell proliferation and differentiation by activating sirt2 and thereby inhibiting NLRP3/caspase-1/GSDMD pathway-mediated skeletal muscle scorpioning, resulting in increased skeletal muscle mass and thus alleviating IR resistance.
  • ||||||||||  Rhein Targets Macrophage SIRT2 to Promote Adipose Tissue Thermogenesis in Obesity (Poster Hall (West A4-B2); 2051) -  May 20, 2024 - Abstract #ADA2024ADA_1703;    
    Rhein promotes adipose tissue thermogenesis by targeting SIRT2 to regulate acetylation-mediated NLRP3 inflammasome activation in macrophages during obesity. Rhein and its derivatives may become potential drug for treating obesity.
  • ||||||||||  MIR181A1HG is a novel long noncoding RNA regulating vascular inflammation and atherosclerosis (Station 9 - Research Gateway) -  May 14, 2024 - Abstract #ESC2024ESC_1431;    
    Deficiency of MIR181A1HG effectively suppressed NLRP3 inflammasome, ECs activation, and atherosclerotic lesion formation. In contrast, EC-specific MIR181A1HG overexpression promoted NLRP3 inflammasome, ECs activation, and atherosclerotic lesion formation, which were reversed by pharmacological inhibition of NLRP3 (MCC950).