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  • ||||||||||  Journal:  Inhibition of Synovial Macrophage Pyroptosis Alleviates Synovitis and Fibrosis in Knee Osteoarthritis. (Pubmed Central) -  Mar 24, 2020   
    In addition, the level of fibrotic markers in synovial fibroblasts were significantly decreased after coculture with siRNA GSDMD-transfected macrophages. To conclude, synovial macrophage pyroptosis may occur in the pathological processes of KOA and inhibition of synovial macrophage pyroptosis alleviates synovitis and fibrosis in KOA model rats.
  • ||||||||||  Journal:  Chronic Gestational Inflammation: Transfer of Maternal Adaptation over Two Generations of Progeny. (Pubmed Central) -  Mar 24, 2020   
    Furthermore, splenocytes stimulated with LPS in vitro exhibited exacerbated inflammatory cytokine responses, which were even more prominent in F2 than F1; this effect could be ascribed to NLRP3 inflammasome hyperactivity in F1 but not F2. Current data illustrates that parental chronic inflammation may mediate the inflammatory profile in offspring, potentially propagating a maladapted proinflammatory phenotype in subsequent generations.
  • ||||||||||  Journal:  Oral Ketone Supplementation Acutely Increases Markers of NLRP3 Inflammasome Activation in Human Monocytes. (Pubmed Central) -  Mar 22, 2020   
    These in vitro and in vivo studies indicate that T-Exo attenuates inflammatory damage caused by ALF and promotes liver tissue repair by inhibiting the activation of the NLRP3 pathway. Measures of NLRP3 activation increased when blood β-OHB was elevated using ketone supplements, suggesting that increasing β-OHB exogenously may have unintended effects that augment inflammatory activation.
  • ||||||||||  Review, Journal:  Genetic Hearing Loss Associated With Autoinflammation. (Pubmed Central) -  Mar 21, 2020   
    The macrophage/monocyte-like cells in the cochlea were also found to be associated with hearing loss in a Slc26a4-insufficient mouse model of human deafness. This review addresses our understanding of genetic hearing loss mediated by autoinflammation and macrophage/monocyte-like cells in the cochlea.
  • ||||||||||  Review, Journal:  NLRP1 and NLRP3 inflammasomes as a new approach to skin carcinogenesis. (Pubmed Central) -  Mar 21, 2020   
    The differences and similarities between these molecular complexes that monitor cellular health, inflammation, and skin carcinogenesis are also highlighted. Despite numerous scientific data, more studies are still required to better understand the biology of inflammasomes in skin cancer development and to explore their therapeutic potential.
  • ||||||||||  Journal:  Estrogen deficiency aggravates apical periodontitis by regulating NLRP3/caspase-1/IL-1β axis. (Pubmed Central) -  Mar 21, 2020   
    Thus, taken all these data together, our results demonstrated that the NLRP3/Caspase-1/IL-1β signaling pathway is involved in the estrogen-mediated apical periodontitis and the consequent bone loss in both human being and animal model. This study may provide a potential target for female apical periodontitis therapy.
  • ||||||||||  Review, Journal:  The modulatory role of dopamine receptors in brain neuroinflammation. (Pubmed Central) -  Mar 19, 2020   
    This review briefly outlined the functions and signaling pathways of DA receptor subtypes as well as its role in inflammation-related glial cells, and subsequently summarized the mechanisms of DA receptors affecting neuroinflammation. Meaningfully, this article provided a theoretical basis for drug development targeting DA receptors in inflammation-related brain diseases.
  • ||||||||||  atorvastatin / Generic mfg.
    Journal:  Statins Promote IL-1β-Dependent Adipocyte Insulin Resistance via Lower Prenylation not Cholesterol. (Pubmed Central) -  Mar 18, 2020   
    Atorvastatin (Lipitor) impaired insulin signaling in adipose tissue from wild-type and IL-18 mice, but not IL-1β mice...Our results show that statin lowering of prenylation isoprenoids activate caspase-1/IL-1β inflammasome responses that impair endocrine control of adipocyte lipogenesis. This may allow targeting of cholesterol-independent statin side-effects on adipose lipid handling without compromising the blood lipid/cholesterol lowering effects of statins.
  • ||||||||||  Journal:  Exosome-like Nanoparticles from Ginger Rhizomes Inhibited NLRP3 Inflammasome Activation. (Pubmed Central) -  Mar 18, 2020   
    Together, the data suggested G-ELNs as new potent agents that block NLRP3 inflammasome assembly and activation. The unique features of G-ELNs including biomolecule protection and tissue bioavailability should facilitate the development of G-ELN-based therapy to target the NLRP3 inflammasome in the disease settings.
  • ||||||||||  Trulicity (dulaglutide) / Eli Lilly
    Journal:  Dulaglutide inhibits high glucose- induced endothelial dysfunction and NLRP3 inflammasome activation. (Pubmed Central) -  Mar 18, 2020   
    Mechanistically, our findings indicate that SIRT1 was involved in this process by showing that knockdown of SIRT1 by transfection with SIRT1 siRNA abolished the inhibitory effects of dulaglutide on IL-1β and IL-18 secretion via suppression of NLRP3, ASC, and p10. These data suggest that dulaglutide might serve as a potential drug for the treatment of cardiovascular complications in T2DM patients.
  • ||||||||||  Journal:  Vibrio pore-forming leukocidin activates pyroptotic cell death via the NLRP3 inflammasome. (Pubmed Central) -  Mar 17, 2020   
    The second step was independent of the inflammasome; however, its mechanism remains unknown. This study sets the foundation for better understanding the immunological consequences of inflammasome activation by a new leukocidin class of toxins, which may be shared between marine bacteria and give rise to new pathogenic isolates.
  • ||||||||||  Review, Journal:  The role of NLRP3 inflammasome in infection-related, immune-mediated and autoimmune skin diseases. (Pubmed Central) -  Mar 17, 2020   
    With the in-depth research, targeting NLRP3 inflammasome and its downstream signaling will provide new insights into the development of future therapeutic strategies. In this review, we summarize the molecular mechanism of NLRP3 inflammasome activation as well as the current knowledge on the contribution of the NLRP3 inflammasome in infection-related, immune-mediated and autoimmune skin diseases.
  • ||||||||||  Review, Journal:  Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways. (Pubmed Central) -  Mar 17, 2020   
    Several studies have showed that inflammasomes are closely related to kidney diseases, especially the NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome, which play a role in regulating kidney inflammation and fibrosis. In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways.
  • ||||||||||  TREK-1 Activation Is Required for Inflammasome Activity Through Augmentation of Macrophage Membrane Polarization (PENNSYLVANIA CONVENTION CENTER, Hall D-E (200 Level), Area G) -  Mar 15, 2020 - Abstract #ATS2020ATS_10114;    
    In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways. Our results suggest that TREK-1 is important in regulating macrophage membrane potential, and may be important in regulating potassium-efflux associated with inflammasome activity.
  • ||||||||||  Heightened ER Stress in Aged Lung Contributes to Dysregulated NLRP3 Inflammasome Activation During Influenza (PENNSYLVANIA CONVENTION CENTER, Hall D-E (200 Level), Area G) -  Mar 15, 2020 - Abstract #ATS2020ATS_9064;    
    IL1RA amplifies RV-induced ILC2 expansion and mucous metaplasia, and IL-1β suppresses it, at least in part by decreasing epithelial cell innate cytokine expression. Data from this study provide new evidence as to why older persons are more susceptible to influenza and provide a possible therapeutic target to decrease morbidity and mortality in this population.
  • ||||||||||  Lipopolysaccharide Causes the Metabolic Flux to Glycolysis and Induces NLRP3 Inflammasome Activation and RIPK3-Mediated Necroptosis in the Lung (PENNSYLVANIA CONVENTION CENTER, Hall D-E (200 Level), Area D) -  Mar 15, 2020 - Abstract #ATS2020ATS_8607;    
    The NLRP3 inflammasome is the dominant processor of IL-1β in human neutrophils, is induced by LPS, and does not require a second signal in these cells. Our findings indicate that LPS leads to altered metabolic flux to glycolysis in lung endothelium, which exacerbates lung ECs necroptosis and NLRP3-mediated inflammasome activation to aggravate lung inflammation and pulmonary vascular injury.This abstract is funded by CURE Grant No: 4100083087
  • ||||||||||  Trim20/Pyrin Regulates Microparticulate Active GasderminD Mediated Cell Injury in Septic Patients (PENNSYLVANIA CONVENTION CENTER, Hall D-E (200 Level), Area D) -  Mar 15, 2020 - Abstract #ATS2020ATS_8578;    
    Our current work provides evidence that activation of RhoA leads to PKN-mediated phosphorylation - dependent pyrin inhibition. Furthermore, this work is the first documentation of pyrin phosphorylation and its inactivation in pro-inflammatory outcomes and microparticulate inflammasome activation in a physiological disease setting.
  • ||||||||||  Melatonin Alleviates Radiation-Induced Lung Injury Via Regulation of Microrna-30e/NLRP3 Axis (PENNSYLVANIA CONVENTION CENTER, Hall D-E (200 Level), Area D) -  Mar 15, 2020 - Abstract #ATS2020ATS_8563;    
    Meanwhile, melatonin exerted its protective effect through negatively regulating the NLRP3 inflammasome in macrophages. The melatonin-mediated miR-30e/NLRP3 signaling may provide novel therapeutic targets for radiation-induced injury.