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  • ||||||||||  Journal:  Leishmania amazonensis Subverts the Transcription Factor Landscape in Dendritic Cells to Avoid Inflammasome Activation and Stall Maturation. (Pubmed Central) -  Apr 7, 2021   
    In conclusion, systems-analyses of our transcriptomics data uncovered important and previously unappreciated changes in the DC transcription factor landscape, thus revealing a novel Leishmania immune subversion strategy directly acting on transcriptional control of gene expression. Our data raise important questions on the dynamic and reciprocal interplay between trans-acting and epigenetic regulators in establishing permissive conditions for intracellular Leishmania infection and polarization of the immune response.
  • ||||||||||  Journal:  Involvement of Asc and Nlrp3 inflammasomes in the testes following spinal cord injury. (Pubmed Central) -  Apr 7, 2021   
    The inflammatory status of HA patients suffering from an ongoing inhibitor includes up-regulated innate immune modulators, which may act as ongoing danger signals that influence the responses to, and eventual outcomes of, ITI therapy. This study provided further evidence of innate immunity activation in testes that could lead to more disruption of spermatogenesis in SCI patients at specific times.
  • ||||||||||  Journal:  Purification, structural characterization, and cognitive improvement activity of a polysaccharides from Schisandra chinensis. (Pubmed Central) -  Apr 7, 2021   
    What's more, mice could improve histopathological changes induced by LPS, suppress the over-activation of glial cells, decrease the expression of proinflammatory cytokines, increase the levels of anti-inflammatory cytokines, reduce the levels of NLRP3, M-caspaes-1, which may further induce the decrease of excessive deposition of Aβ. Furthermore, SCP2-1 could inhibit the over-activation of NF-κB and the hyperphosphorylation of P38 MAPK pathway.
  • ||||||||||  Lynparza (olaparib) / Merck (MSD), AstraZeneca
    Preclinical, Journal:  Modulation of Inflammasome and Pyroptosis by Olaparib, a PARP-1 Inhibitor, in the R6/2 Mouse Model of Huntington's Disease. (Pubmed Central) -  Apr 7, 2021   
    Our results indicate that Olaparib administration starting from the pre-symptomatic stage of the neurodegenerative disease increased survival, ameliorated the neurological deficits, and improved clinical outcomes in neurobehavioral tests mainly by modulating the inflammasome activation. These results suggest that Olaparib, a commercially available drug already in use as an anti-neoplastic compound, exerts a neuroprotective effect and could be a useful pharmaceutical agent for Huntington's disease therapy.
  • ||||||||||  Review, Journal:  Inhibiting the NLRP3 Inflammasome. (Pubmed Central) -  Apr 7, 2021   
    This review focuses on the structural basis and mechanism for NLRP3 inflammasome signaling in the context of drug design, providing chemical structures, activities, and clinical potential of direct inflammasome inhibitors. A cryo-EM structure of NLRP3 bound to NEK7 protein provides structural insight and aids in the discovery of novel NLRP3 inhibitors utilizing ligand-based or structure-based approaches.
  • ||||||||||  Review, Journal:  Monounsaturated Fatty Acids in Obesity-Related Inflammation. (Pubmed Central) -  Apr 7, 2021   
    In this review, we describe the molecular effects of specific classes of fatty acids (saturated and unsaturated) to better understand the impact of different diets (Western versus Mediterranean) on inflammation in a metabolic context. Given the beneficial effects of a MUFA-rich Mediterranean diet, we also present the most recent data on the role of SCD1 activity in the modulation of SFA-induced chronic inflammation.
  • ||||||||||  Clinical, Review, Journal:  Perinatal Infection: A Major Contributor to Efficacy of Cooling in Newborns Following Birth Asphyxia. (Pubmed Central) -  Apr 7, 2021   
    Hypothermia stimulates microglia to secret cold-inducible RNA-binding protein (CIRP), which triggers NF-κB, controlling multiple inflammatory pathways, including nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasomes and cyclooxygenase-2 (COX-2) signaling. Brain responses through changes in heat shock protein and cold shock protein transcription and gene-expression following fever range and hyperthermia may be new promising potential therapeutic targets.
  • ||||||||||  Journal:  AIM2 in regulatory T cells restrains autoimmune diseases. (Pubmed Central) -  Apr 7, 2021   
    Lineage-tracing analysis demonstrates that AIM2 promotes the stability of T cells during inflammation. Although AIM2 is generally accepted as an inflammasome effector in myeloid cells, our results demonstrate a T cell-intrinsic role of AIM2 in restraining autoimmunity by reducing AKT-mTOR signalling and altering immune metabolism to enhance the stability of T cells.
  • ||||||||||  CH-223191 / BMS
    Journal:  Aryl Hydrocarbon Receptor is Involved in the Proinflammatory Cytokine Response to Cadmium. (Pubmed Central) -  Apr 7, 2021   
    The involvement of AhR signaling in the effects of Cd on the interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF) lung leukocyte response was investigated in vitro using the receptor antagonist CH-223191...AhR signaling is involved in the lung leukocyte proinflammatory cytokine response to Cd. The relevance of the AhR to the cytokine response to Cd provides new insight into the mechanisms of Cd immunotoxicity.
  • ||||||||||  colchicine / Generic mfg.
    Preclinical, Journal:  Effect of extract of Quzhou Aurantii Fructus on hepatic inflammation and NF-κB/NLRP3 inflammasome pathway in CCl_4-induced liver fibrosis mice (Pubmed Central) -  Apr 7, 2021   
    Totally 60 C57 BL/6 male mice were randomly divided into control group(distilled water, oral), model group(distilled water, oral), colchicines group(Col, colchicines 2 mg·kg~(-1)·d~(-1), oral), low-dose QAF group(QAF-L, QAF 100 mg·kg~(-1)·d~(-1), oral) and high-dose QAF group(QAF-H, QAF 300 mg·kg~(-1)·d~(-1), oral) by random number table method...In conclusion, QAF improves CCl_4-induced liver fibrosis in mice. The mechanism may be related to the inhibition of NF-κB/NLRP3 inflammasome-mediated inflammation signaling pathway.
  • ||||||||||  Review, Journal:  The Role of the Interplay Between Autophagy and NLRP3 Inflammasome in Metabolic Disorders. (Pubmed Central) -  Apr 7, 2021   
    In recent years, the interplay between autophagy and NLRP3 inflammasome has been reported to contribute to many diseases including metabolic disorders related diseases. In this review, we summarized the recent studies on the interplay between autophagy and NLRP3 inflammasome in metabolic disorders to provide ideas for the relevant basic research in the future.
  • ||||||||||  Journal, IO biomarker:  The Impact of Melatonin and NLRP3 Inflammasome on the Expression of microRNAs in Aged Muscle. (Pubmed Central) -  Apr 7, 2021   
    The lack of NLRP3 inflammasome also improved the skeletal muscle fibers arrangement and reduced the collagen deposits compared with WT muscle during aging. For the first time, we showed that melatonin significantly reduced the expression of miR-21, miR-146a, and miR-223 (p < 0.05 for all ones, and p < 0.01 for miR-21 at 24 months old) in aged WT mice, increased miR-223 in NLRP3 mice (p < 0.05), and induced miR-483 expression in both mice strains, this increase being significant at 24 months of age.
  • ||||||||||  azathioprine / Generic mfg.
    Preclinical, Journal:  Long-Term Treatment of Azathioprine in Rats Induces Vessel Mineralization. (Pubmed Central) -  Apr 7, 2021   
    As the AZA effect could be decreased in NLRP3 aortic rings in an ex vivo experiment, the signaling pathway might be, at least in part, dependent on the NLRP3 inflammasome. Although human studies are necessary to confirm the harmful effects of AZA on vascular stiffening, these results provide further evidence of induction of VSMC calcification under AZA treatment and its effects on vessel structure.
  • ||||||||||  Review, Journal:  From Mitochondria to Atherosclerosis: The Inflammation Path. (Pubmed Central) -  Apr 7, 2021   
    Primary or secondary mitochondrial dysfunctions are associated with the initiation and progression of atherosclerosis by elevating the production of ROS, altering mitochondrial dynamics and energy supply, as well as promoting inflammation. Knowing and understanding the pathways behind mitochondrial-based inflammation in atheroma progression is essential to discovering alternative or complementary treatments.
  • ||||||||||  Review, Journal:  Activation and Inhibition of the NLRP3 Inflammasome by RNA Viruses. (Pubmed Central) -  Apr 7, 2021   
    On the other hand, several viruses use virus-encoded proteins to suppress inflammation activation, such as the influenza virus NS1 protein and the measles virus (MV) V protein. In this review, we summarize how RNA virus infection leads to the activation or inhibition of the NLRP3 inflammasome.
  • ||||||||||  [VIRTUAL] Shaperon Inc. () -  Apr 3, 2021 - Abstract #BIO2021BIO_119;    
    Its novel MoA of inflammasome inhibition through GPCR-P2X7 modulation provides a solution to inherent shortcomings of current inflammasome inhibitors. • suppresses not only IL-1b but TNF-a, IL-6, and other major pro-inflammatory cytokines • overcomes inherent shortcomings of conventional P2X7 antagonists and NLRP3 inhibitors such as off-target effects, polymorphism, and redundant pro-inflammatory pathways etc. • induces immune regulatory circuit by increasing the number of Treg and MDSCs • most advanced development pipelines among peers - phase 2 in atopic dermatitis (topical) ongoing - phase 2 in Covid 19 pneumonia (IV) ongoing - phase 1 in sepsis completed - pre-clincial stage in Alzheimer's disease, ulerative colitis, NASH (oral)
  • ||||||||||  Preclinical, Journal:  Structural characteristics of a mannoglucan isolated from Chinese yam and its treatment effects against gut microbiota dysbiosis and DSS-induced colitis in mice. (Pubmed Central) -  Apr 2, 2021   
    Oral administration of CYP-1 dramatically alleviated colonic pathological damage, suppressed the activation of colonic inflammatory signaling pathways (such as NF-κB and NLRP3 inflammasome), recovered the mRNA expression of junctional proteins (such as ZO-1, claudin-1, occludin, and connexin-43), and modulated the gut microbiota by decreasing the abundances of Alistipes, Helicobacter, and an unidentified Enterobacteriaceae, in DSS-induced colitis mice. Overall, the present study elucidated that a new polysaccharide structure CYP-1 from Chinese yam and its therapeutic potential as a prebiotic for the prevention of inflammatory bowel disease.
  • ||||||||||  Review, Journal:  Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology. (Pubmed Central) -  Apr 2, 2021   
    Elevated levels of extracellular ATP induced by SARS-CoV-2 infection may trigger hyperactivation of P2X7 receptors leading to NLRP3 inflammasome stimulation as a key mediator of neuroinvasion and consequent neuroinflammatory processes, as observed in psychiatric disorders and neurodegenerative diseases. In this context, P2X7 receptor antagonism could be a promising strategy to prevent or treat neurological complications in COVID-19 patients.
  • ||||||||||  Journal:  Mycobacterium tuberculosis infection up-regulates MFN2 expression to promote NLRP3 inflammasome formation. (Pubmed Central) -  Apr 2, 2021   
    Furthermore, we found that MTB stimulation by MTB-specific antigen ESAT-6 or lysate of MTB promoted MFN2 interaction with NLRP3 inflammasomes, resulting in the assembly and activation of the inflammasome and, subsequently, IL-1β secretion. These findings suggest that MFN2 and mitochondria play important role in the pathogen-host interaction during MTB infection.
  • ||||||||||  Journal:  The P2X Receptor in Microglial Cells Modulates the Endolysosomal Axis, Autophagy, and Phagocytosis. (Pubmed Central) -  Apr 2, 2021   
    In summary, the P2X receptor modulates clearance of extracellular debris by microglial cells and mediates lysosomal damage that can activate the NLRP3 inflammasome. A better understanding of how the P2X receptor alters phagocytosis, lysosomal health, inflammation, and autophagy can lead to therapies that balance the inflammatory and clearance roles of microglial cells.
  • ||||||||||  Review, Journal:  The NLRP3 Inflammasome as a Critical Actor in the Inflammaging Process. (Pubmed Central) -  Apr 1, 2021   
    However, one specific shared feature seems to be of capital relevance for most of these conditions: the low-grade chronic inflammatory state inherently associated with aging, i.e., inflammaging. Here, we review the molecular and cellular mechanisms that link aging and inflammaging, focusing on the role of the innate immunity and more concretely on the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, as well as how the chronic activation of this inflammasome has a detrimental effect on different age-related disorders.
  • ||||||||||  colchicine / Generic mfg.
    Preclinical, Journal:  Gene-Dose Effect of MEFV Gain-of-Function Mutations Determines ex vivo Neutrophil Activation in Familial Mediterranean Fever. (Pubmed Central) -  Apr 1, 2021   
    Co-culture with colchicine and/or stimulation with adenosine triphosphate (ATP) and lipopolysaccharide (LPS) led to a significant increase in receptor shedding...In summary, the data demonstrate that ex vivo cultured neutrophils derived from FMF patients display a unique phenotype with spontaneous release of high amounts of IL-18, S100A12, MPO, caspase-1, and proteinase 3 and spontaneous activation as demonstrated by the loss of CD62L. Neutrophilic activation seems to be independent from IL-1 activation and displays a gene-dose effect that may be responsible for genotype-dependent phenotypes.
  • ||||||||||  Review, Journal:  Health disparities: Intracellular consequences of social determinants of health. (Pubmed Central) -  Apr 1, 2021   
    The relevance of this conceptual and theoretical model considering the SARS-CoV-2 pandemic are highlighted. Finally, the case of asthma is presented as a chronic condition that is modified by adverse SDOH exposures and is manifested through the dysregulation of immune cell redox regulatory process we highlight in this review.