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- [VIRTUAL] Single-cell and spatial transcriptomics reveal NLRP3 inflammasome-mediated immune-stromal interactions during vasculitis and cardiovascular inflammation. () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1763;
In addition, pharmacological inhibition of NLRP3 prevented the development of cardiovascular inflammation. Our results unravel the cellular diversity involved in IL-1β production and signaling in KD cardiovascular lesions and demonstrate that therapeutic strategies targeting NLRP3 might be beneficial for human KD.
- [VIRTUAL] Hemozoin-mediated, dendritic cell-intrinsic inflammasome activation limits long-lived anti-malarial immunity () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1737;
Mechanistically, we identified that dendritic cell-intrinsic NLRP3 inflammasome activation reduced conventional type 1 dendritic cell survival, phagocytosis and T cell priming functions in vivo. These data identify previously unappreciated consequences of hemozoin deposition during malaria and highlight the capacity of the malarial pigment to effectively program immune evasion during the earliest events following an initial Plasmodium exposure.
- [VIRTUAL] Histone deacetylase-1 controls IL-1β production through the regulation of NLRP3 expression and activation in tuberculosis infection () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1724;
Treatment of low dose aerosol Mtb-infected mice with HDAC-1 inhibitor increased IL-1β in mice lungs without affecting IL-6 production. These suggest that HDAC-1 controls IL-1β maturation via regulation of NLRP3 expression and activation, thus suggesting a novel mechanism for the regulation of IL-1β, a major inflammatory cytokine in tuberculosis infection and other inflammatory diseases.
- [VIRTUAL] Combination of dmLT and MPL-A adjuvants synergistically and differentially activates the canonical inflammasome in DCs and macrophages in the absence of pyroptosis () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1705;
Furthermore, RNA sequencing and ingenuity pathway analysis support that the combination adjuvant may allow these DCs to polarize a multi-faceted Th1/2/17 CD4 T cell response. Because macrophages and DCs have distinct roles in the interface between innate and adaptive immunity, understanding the cellular and molecular actions of adjuvants on these cells is critical when developing new vaccines.
- clindamycin phosphate / Generic mfg.
[VIRTUAL] NLRP3 inflammasome inhibitor as an adjunct host-directed therapy in a hyper susceptible mouse model of Group A Streptococcal Necrotizing Fasciitis. () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1702;
To fine-tune IL-1b levels while simultaneously attenuating GAS multiplication and toxin synthesis, here, we investigated the effect of MCC950 (MCC), a small molecule inhibitor for NLRP3 inflammasome activation as a host-directed adjunct to clindamycin (CLN) (10mg/kg each, everyday X 5 days) in a mouse model of GAS NF...These results indicate that NLRP3 inflammasome activation may be primarily involved in excess IL-1b release, neutrophil influx, and tissue damage during GAS-NF. The evidence of improved outcomes suggests, in part, a beneficial efficacy of MCC950 to target NLRP3 as a feasible adjunct to CLN and mitigate inflammation and pathology with no adverse effects or delayed toxicity
- [VIRTUAL] NLRP3 and AIM2 inflammasome-triggered Th17 cell response promotes severe immunopathology in schistosomiasis () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1672;
We also determined that inflammasome-induced IL-1β promotes the anti-inflammatory Th2 cytokine IL-4. Our findings establish NLRP3 and AIM2 inflammasomes as central inducers of pathogenic Th17 responses in schistosomiasis.
- [VIRTUAL] Understanding NLRs and AIM2 cellular and molecular signalling in glioblastoma pathophysiology () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1649;
Our results characterize novel cell specific differential expression and signalling profile of several NLR genes (including NLRP3, NLRP12 and ASC) in microglia, astrocytes, endothelial cells and the tumour cell populations in GBM patient tissue. We provide critical insights into innate immune signalling within the GBM microenvironment and identify key markers for future therapeutic interventions.
- [VIRTUAL] CCN3 aggravates intestinal inflammation in inflammatory colitis through regulating NLRP3 inflammasome in macrophages () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1648;
In addition, we found that the production of IL-1b and expression of NLRP3 in LysMCre-ccn3f/f bone marrow-derived macrophages (BMDM) were significantly lower than those in LysMCre, indicating that NLRP3 inflammasome activation may be involved. In conclusion, our data provide a direct evidence that CCN3 may play a role in colitis by regulating NLRP3 inflammasome activation in macrophages.
- [VIRTUAL] The lncRNA Neat1 promotes activation of NLRP3 inflammasome in macrophages () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1217;
- [VIRTUAL] Itaconate confers tolerance to late NLRP3 inflammasome activation () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1117;
Mechanistically, itaconate accumulation upon prolonged inflammatory stimulation prevents full caspase-1 activation and processing of gasdermin D, which we demonstrate to be post-translationally modified by endogenous itaconate. Altogether, our data demonstrate that metabolic rewiring in inflammatory macrophages establishes tolerance to NLRP3 inflammasome activation which, if uncontrolled, can result in pyroptotic cell death and tissue damage.
- [VIRTUAL] Citrin, a mitochondrial transporter, interacts with NLRP3 and regulates inflammasome activity () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1116;
Importantly, this regulation was specific to NLRP3 and did not affect the AIM2 inflammasome or other cell death pathways. Altogether, our studies reveal a novel role for Citrin in regulation of the NLRP3 inflammasome and inflammatory cytokine release.
- [VIRTUAL] Mitochondrial calcium uniporter positively regulates phagocytosis-dependent activation of NLRP3 inflammasome () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1113;
Furthermore, McuΔmye mice showed attenuated inflammatory response and tissue damage in a chemically induced colitis model. In sum, our results identify a novel function and mechanism of MCU in regulating phagocytosis-dependent NLRP3 inflammatory response.
- [VIRTUAL] Chronic air pollution exposure exaggerates obesity-induced tissue inflammation and insulin resistance by activating inflammasome () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_1068;
In sum, our results identify a novel function and mechanism of MCU in regulating phagocytosis-dependent NLRP3 inflammatory response. Our data suggest that NLRP3 inflammasome activation mediates air pollution-induced tissue inflammation and insulin resistance.
- [VIRTUAL] AIM2 in regulatory T cells restrains autoimmune diseases () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_906;
Mechanistically, AIM2 interacts with the RACK1/PP2A-phosphatase complex to restrain Akt-phosphorylation. While AIM2 is generally accepted as an inflammasome effector in myeloid cells, this report unveils a T cell-intrinsic role of AIM2 in restraining autoimmunity by diminishing Akt-mTOR signaling and altering immune-metabolism to enhance Treg stability.
- [VIRTUAL] Single-cell and spatial transcriptomics reveal NLRP3 inflammasome-mediated immune-stromal interactions during vasculitis and cardiovascular inflammation. () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_699;
In addition, pharmacological inhibition of NLRP3 prevented the development of cardiovascular inflammation. Our results unravel the cellular diversity involved in IL-1β production and signaling in KD cardiovascular lesions and demonstrate that therapeutic strategies targeting NLRP3 might be beneficial for human KD.
- [VIRTUAL] AIM2 in regulatory T cells restrains autoimmune diseases () - May 19, 2021 - Abstract #IMMUNOLOGY2021IMMUNOLOGY_487;
Mechanistically, AIM2 interacts with the RACK1/PP2A-phosphatase complex to restrain Akt-phosphorylation. While AIM2 is generally accepted as an inflammasome effector in myeloid cells, this report unveils a T cell-intrinsic role of AIM2 in restraining autoimmunity by diminishing Akt-mTOR signaling and altering immune-metabolism to enhance Treg stability.
- [VIRTUAL] CD47-Mediated Gli1/Notch1 Signaling is a Key Regulator of Mesenchymal Stem Cell Immunomodulation in Liver Inflammatory Injury () - May 18, 2021 - Abstract #ATC2021ATC_2290;
NICD is a novel coactivator of Gli1, and the target gene Dvl2 regulated by the NICD-Gli1 complex is crucial for the modulation of NLRP3-driven inflammatory response in MSC-mediated immune regulation. Our findings provide novel potential therapeutic targets in MSC-based immunotherapy of sterile inflammatory liver injury.
- [VIRTUAL] Myeloid Foxo1-β-catenin Axis Regulates Hedgehog/Gli1 Signaling and Controls NLRP3-Mediated Innate Immune Responses in Sterile Inflammatory Liver Injury () - May 18, 2021 - Abstract #ATC2021ATC_1941;
Myeloid-specific Foxo1 deficiency promotes the Hedgehog/Gli1 signaling and mitigates IR-induced hepatocellular injury through disruption of nuclear Foxo1-β-catenin interaction, which in turn enhances β-catenin/TCF binding and activates the Hedgehog/Gli1/Snail signaling, resulting in reduced NEK7/NLRP3-driven liver inflammation and RIPK3-mediated hepatocyte necroptosis. Our findings underscore the crucial role of myeloid Foxo1 signaling in the modulation of NLRP3-mediated innate immunity and inflammatory responses during sterile inflammatory liver injury, and imply the therapeutic potential in organ IRI and transplant recipients.
- [VIRTUAL] Myeloid YAP-HSF1 Signaling Inhibits NLRP3 Function and RIPK3-mediated Hepatocyte Necroptosis in Liver Ischemia and Reperfusion Injury () - May 18, 2021 - Abstract #ATC2021ATC_1243;
HSF1 is required for the myeloid YAP-mediated immune regulation in liver IRI. Our findings demonstrate the key mechanistic role of myeloid YAP in liver inflammatory injury, and provide novel therapeutic potential in organ IRI and transplant recipients.
- [VIRTUAL] NLRP3 inflammasomes contribute to dysregulated sleep and electroencephalogram delta power after mild and moderate TBI in mice () - May 17, 2021 - Abstract #SLEEP2021SLEEP_237;
These effects were evident by significant increased frequencies of waking episodes induced by the TBIs. Conclusion Our findings suggest that NLRP3 inflammasomes contribute to dysregulated sleep occurring acutely or more persistently after TBI.
- | Journal: ADSCs inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation. (Pubmed Central) - May 15, 2021
Conclusion Our findings suggest that NLRP3 inflammasomes contribute to dysregulated sleep occurring acutely or more persistently after TBI. These results demonstrated that ADSCs could restore skin barrier function at the cellular and structural levels, enhance hair follicle stem cell (HFSCs) activity by regulating TGF-β2 and inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation.
- | Ilaris (canakinumab) / Novartis
Journal: Residual inflammatory risk associated with interleukin-18 and interleukin-6 after successful interleukin-1β inhibition with canakinumab: further rationale for the development of targeted anti-cytokine therapies for the treatment of atherothrombosis. (Pubmed Central) - May 15, 2021
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These results demonstrated that ADSCs could restore skin barrier function at the cellular and structural levels, enhance hair follicle stem cell (HFSCs) activity by regulating TGF-β2 and inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation. There remains substantial residual inflammatory risk related to both IL-18 and IL-6 after IL-1β inhibition with canakinumab These data support further pharmacologic development of therapies for atherothrombosis that target IL-18 or IL-6 signalling, or that can simultaneously inhibit both IL-1β and IL-18 (such as NLRP3 inflammasome inhibitors).
- | Journal: MiR-135b protects cardiomyocytes from infarction through restraining the NLRP3/caspase-1/IL-1β pathway. (Pubmed Central) - May 15, 2021
There remains substantial residual inflammatory risk related to both IL-18 and IL-6 after IL-1β inhibition with canakinumab These data support further pharmacologic development of therapies for atherothrombosis that target IL-18 or IL-6 signalling, or that can simultaneously inhibit both IL-1β and IL-18 (such as NLRP3 inflammasome inhibitors). The present findings shed light on the protective role of miR-135b in MI mediated by the inhibition of the NLRP3/caspase-1/IL-1β pathway.
- | Journal, IO biomarker: The molecular mechanisms of excessive hippocampal endoplasmic reticulum stress depressing cognition-related proteins expression and the regulatory effects of Nrf2. (Pubmed Central) - May 15, 2021
On the other hand, both 4-PBA and TBHQ reduced ER stress and reversed the expression of the above-mentioned proteins. Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1β pathway, which could be reversed by activated Nrf2-HO-1 pathway.
- | Preclinical, Journal: IL-1β prevents ILC2 expansion, type 2 cytokine secretion and mucus metaplasia in response to early-life rhinovirus infection in mice. (Pubmed Central) - May 15, 2021
Macrophage IL-1β limits type 2 inflammation and mucous metaplasia following RV infection by suppressing epithelial cell innate cytokine expression. Reduced IL-1β production in immature animals provides a mechanism permitting asthma development after early-life viral infection.
- | Journal: Dermal fillers do not induce upregulation of NLRP3 inflammasomes or expression of inflammatory cytokines in granulomas. (Pubmed Central) - May 15, 2021
No increased inflammasome activation could be observed; however, filler granulomas were infiltrated with granulocytes and macrophages. Therefore, we speculate that an unspecific immune response might be the key player in the formation of filler granuloma.
- | Preclinical, Journal: HDAC10 alleviates inflammation after intracerebral hemorrhage via the PTPN22/NLRP3 pathway in rats. (Pubmed Central) - May 15, 2021
Our study demonstrated that HDAC10 silencing aggravated NLRP3-mediated inflammatory responses after ICH in rats via the PTPN22 pathway. These results suggest that regulating the NLRP3 inflammasome may be a novel method to ameliorate ICH injury.
- | Journal: Role of Parkin-mediated mitophagy in the protective effect of polydatin in sepsis-induced acute kidney injury. (Pubmed Central) - May 15, 2021
These results suggest that regulating the NLRP3 inflammasome may be a novel method to ameliorate ICH injury. These findings indicate that Parkin-mediated mitophagy is important for the protective effect of PD in SI-AKI, and the underlying mechanisms include the inhibition of mitochondrial dysfunction and NLRP3 inflammasome activation.
- | Preclinical, Journal: Soyasaponin II protects against acute liver failure through diminishing YB-1 phosphorylation and Nlrp3-inflammasome priming in mice. (Pubmed Central) - May 15, 2021
Finally, immunofluorescence analysis showed elevated p-YB-1 nuclear translocation in macrophages of acute liver failure patients compared to controls. Our data shows that soyasaponin II which serves as a novel inhibitor for YB-1 phosphorylation and Nlrp3 inflammasome priming could protect mice against LPS/GalN induced acute liver failure.
- | Journal: Autophagy promotes phagocytosis and clearance of Treponema pallidum via the NLRP3 inflammasome in macrophages. (Pubmed Central) - May 15, 2021
The NLRP3 inflammasome modulates autophagy and phagocytosis in vitro. These data may be useful for understanding the host-pathogen relationship and establish the groundwork for strategies to combat syphilis.
- | Journal: Mechanistic Differences in Cell Death Responses to Metal-Based Engineered Nanomaterials in Kupffer Cells and Hepatocytes. (Pubmed Central) - May 15, 2021
Interestingly, although V O induces IL-1β release and delays caspase 1 activation by vanadium ion interference in membrane Na /K adenosine triphosphate (ATP)ase activity, the major cell death mechanism in KC (and Hepa 1-6) is caspase 3 mediated apoptosis. These findings improve the understanding of the mechanisms of metal-based engineered nanomaterial (ENM) toxicity in liver cells toward comprehensive safety evaluation.
- || Review, Journal: Gout: a disease involved with complicated immunoinflammatory responses: a narrative review. (Pubmed Central) - May 15, 2021
And the immune cells in gout, including neutrophils, monocytes/macrophages, and lymphocytes, all play important roles in the pathogenesis of gout. In this review, we mainly emphasize the understanding of various cytokines, inflammasome, and immune cells involved in the onset of gout, in order to provide a systematic and theoretical basis for the novel exploration of inflammatory therapeutic targets for gout.
- || Enbrel (etanercept) / Pfizer, Amgen
Clinical, Journal: Tumor necrosis factor-alpha blockade ameliorates inflammatory response in two children with chronic infantile neurological, cutaneous and articular syndrome. (Pubmed Central) - May 15, 2021
Anti-TNF-α (etanercept) therapy successfully alleviated both clinical symptoms and systemic inflammation after 6 months. These results suggest the complexity of the mechanisms of the disease and that TNF-α blockade will broaden the therapeutic approach for a subset of patients.
- | Preclinical, Journal: Down-regulation of DJ-1 augments neuroinflammation via Nrf2/Trx1/NLRP3 axis in MPTP-induced Parkinson's disease mouse model. (Pubmed Central) - May 15, 2021
Taken together, these data suggested that down-regulation of DJ-1 accelerated microglia-mediated neuroinflammation and cell apoptosis via Nrf2/Trx1/NLRP3 axis. Thus, our results demonstrated the important role of DJ-1 in PD pathogenesis and warranted further investigation of DJ-1 as a therapeutic target for PD.
- | Journal: Arsenic induces hepatic insulin resistance via mtROS-NLRP3 inflammasome pathway. (Pubmed Central) - May 15, 2021
Furthermore, mitochondrial reactive oxygen species (mtROS) scavenger alleviated the upregulated ox-mtDNA and mitophagy, thereby inhibiting the NLRP3 inflammasome activation, and improving insulin signaling. Taken together, these data demonstrated that mtROS-triggered ox-mtDNA, mitophagy, and the activation of NLRP3 inflammasome was involved in arsenic-induced hepatic IR.
- || Remicade (infliximab) / Merck (MSD), Mitsubishi Tanabe, J&J, Ilaris (canakinumab) / Novartis
Clinical, Review, Journal: A case of cryopyrin-associated periodic fever syndrome during canakinumab administration complicated by inflammatory bowel disease. (Pubmed Central) - May 15, 2021
To the best of our knowledge, this is the first report of a case of inflammatory bowel disease secondary to CAPS complicated by gastrointestinal symptoms and arthritis which canakinumab could not control. Patients with CAPS who have symptoms that cannot be controlled by canakinumab should be considered for possible co-morbidities.
- | colchicine / Generic mfg.
Journal: Colchicine Alleviates Cholesterol Crystal-Induced Endothelial Cell Pyroptosis through Activating AMPK/SIRT1 Pathway. (Pubmed Central) - May 15, 2021
However, the above effects of colchicine were completely offset by the treatment of siRNA targeting AMPKα and Sirtuin1 (SIRT1). Therefore, we conclude that colchicine plays a crucial role in alleviating the intracellular inflammatory response and NLRP3 inflammation activation, attenuating the levels of cellular oxidative stress and pyroptosis in endothelial cells via regulating AMPK/SIRT1 signaling, which may be a concrete mechanism for the secondary prevention of cardiovascular diseases.
- | Preclinical, Journal: Geniposide alleviates diabetic nephropathy of mice through AMPK/SIRT1/NF-κB pathway. (Pubmed Central) - May 15, 2021
The protein expressions in APMK/SIRT1/NF-κB pathway were significantly decreased by GE treatment. These results suggested that GE could efficiently block oxidative stress and inflammatory responses accompanied with pyroptosis, thus inhibiting the development of DN, and its mechanism might be related to APMK/SIRT1/NF-κB pathway.
- | dexmedetomidine / Generic mfg.
Preclinical, Journal: Dexmedetomidine attenuates ventilator-induced lung injury in rats by up-regulating NLRC3. (Pubmed Central) - May 15, 2021
These results suggested that GE could efficiently block oxidative stress and inflammatory responses accompanied with pyroptosis, thus inhibiting the development of DN, and its mechanism might be related to APMK/SIRT1/NF-κB pathway. This study demonstrates that NLRC3 is involved in the VILI of rats, and dexmedetomidine can attenuate the VILI in rats by up-regulating the expression level of NLRC3.
- || Review, Journal: NLRP3 Inflammasomes in Parkinson's disease and their Regulation by Parkin. (Pubmed Central) - May 15, 2021
Evidence has confirmed a relationship between Parkin and NLRP3 inflammasomes. In this review, we summarize the current understanding of NLRP3 inflammasomes and their role in PD progression, and discuss their regulation by Parkin.
- | Journal: Fullerene nanoparticles: a promising candidate for the alleviation of silicosis-associated pulmonary inflammation. (Pubmed Central) - May 15, 2021
Further investigations reveal that FNs could effectively inhibit the activation of NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome, and thus prevent the secretion of mature IL-1β and neutrophil influx, deriving from the superior ROS scavenging capability. Importantly, FNs could not cause any obvious toxicity after pulmonary administration.
- | Journal: HIF-1α induces NLRP3 expression by M1 macrophages in non-eosinophilic chronic rhinosinusitis with nasal polyps. (Pubmed Central) - May 15, 2021
Importantly, FNs could not cause any obvious toxicity after pulmonary administration. No abstract available
- | Journal: Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B. (Pubmed Central) - May 15, 2021
NF-κB inhibitor and CRISPR-Cas9-mediated knockout of LC3B attenuated the effects of combination which indicated nontoxic-dose DON aggravated LPS-induced intestinal inflammation and tight junction disorder through activating NF-κB signaling pathway and autophagy-related protein LC3B. It further warns that ingesting low doses of mycotoxins may exacerbate the effects of intestinal pathogens on the body.
- |||||| dapansutrile (OLT-1177) / Olatec Therap
Clinical: Congrats @AbbateAntonio on your @FralinLifeSci seminar on #inflammation, #Interleukin1blockade and #heartdisease. Impactful translational research within #IL1 and #NLRP3. Olatec is honored to collaborate with you in trials with #NLRP3inhibitor dapansutrile and @VCUHealthHeart! https://t.co/LWmSITgiJf (Twitter) - May 15, 2021
- | Journal: Hypoxia Inducible Factor-1α (HIF-1α) Mediates NLRP3 Inflammasome-Dependent-Pyroptotic and Apoptotic Cell Death Following Ischemic Stroke. (Pubmed Central) - May 15, 2021
We found that HIF-1α likely regulates inflammatory responses through the NLRP3 inflammasome complex, thus influencing both apoptotic and pyroptotic cell death after stroke. These findings suggest that future investigations are needed regarding HIF-1α and its role as a potential molecular target in the treatment of acute ischemic stroke.
- | Journal: Activated protein C and PAR1-derived and PAR3-derived peptides are anti-inflammatory by suppressing macrophage NLRP3 inflammasomes. (Pubmed Central) - May 15, 2021
These findings suggest that future investigations are needed regarding HIF-1α and its role as a potential molecular target in the treatment of acute ischemic stroke. The results indicate that both APC and certain PAR1-derived and PAR3-derived peptides which are biased agonists for PAR1 or PAR3 can reduce inflammasome activity in stimulated human monocytes as measured by caspase-1 activity and IL-1β release and that PAR-derived biased peptide agonist combinations are synergistically anti-inflammatory.
- | Journal, IO biomarker: Amorphous silica nanoparticles induce inflammation via activation of NLRP3 inflammasome and HMGB1/TLR4/MYD88/NF-kb signaling pathway in HUVEC cells. (Pubmed Central) - May 15, 2021
Subsequently, toll-like receptor 4 (TLR4) could bind with HMGB1, up-regulate the expression of myeloid differentiation factor 88 (MyD88) and then activate nuclear factor kappa-B (NF-κB) signaling pathway, ultimately induced the inflammatory response of HUVECs. Overall, out results revealed the related signaling pathways of cell inflammation induced by amorphous SiO NPs, which provided new insights in understanding SiO NPs-induced cytotoxicity and offered safety guidance for further nanomaterial application.
- | Journal: Melatonin attenuates AFB1-induced cardiotoxicity via the NLRP3 signalling pathway. (Pubmed Central) - May 15, 2021
Overall, out results revealed the related signaling pathways of cell inflammation induced by amorphous SiO NPs, which provided new insights in understanding SiO NPs-induced cytotoxicity and offered safety guidance for further nanomaterial application. Melatonin may reduce NLRP3 inflammasome activation by inhibiting oxidative stress and thus protect against injury from AFB1-induced myocardial toxicity.
- || Review, Journal: The Long Non-coding RNAs: Paramount Regulators of the NLRP3 Inflammasome. (Pubmed Central) - May 15, 2021
The present review is a novel attempt to consolidate the substantial role of lncRNAs in the regulation of the NLRP3 inflammasome. A deeper insight on the NLRP3 inflammasome regulation by lncRNAs will help in developing targeted and beneficial therapeutics in the future.
- || Review, Journal, IO biomarker: Overview of the molecular determinants contributing to the expression of Psoriasis and Psoriatic Arthritis phenotypes. (Pubmed Central) - May 15, 2021
In addition, special emphasis will be given to the contribution of epigenetic elements (methylation pattern, non-coding RNAs, chromatin modifiers and 3D genome organization) to the etiopathogenesis and progression of psoriasis and psoriatic arthritis. The evidence discussed in this review highlights how the knowledge of patients' clinical and (epi)genomic make-up could be helpful for improving the available therapeutic strategies for psoriasis and psoriatic arthritis treatment.