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#inflammasome — Public Fediverse posts

Live and recent posts from across the Fediverse tagged #inflammasome, aggregated by home.social.

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  1. Statins may trigger muscle side effects by activating inflammatory danger signals

    New experimental findings reveal how statins may push vulnerable muscle cells into a stress state, suggesting future strategies…
    #NewsBeep #News #Technology #AU #Australia #Cell #cholesterol #Glycolysis #Healthcare #Heart #Inflammasome #Leucine #Lipoprotein #Muscle #muscleatrophy #Nucleotide #protein #Statin #stress #therapy
    newsbeep.com/au/754336/

  2. Statins may trigger muscle side effects by activating inflammatory danger signals

    New experimental findings reveal how statins may push vulnerable muscle cells into a stress state, suggesting future strategies…
    #NewsBeep #News #Technology #AU #Australia #Cell #cholesterol #Glycolysis #Healthcare #Heart #Inflammasome #Leucine #Lipoprotein #Muscle #muscleatrophy #Nucleotide #protein #Statin #stress #therapy
    newsbeep.com/au/754336/

  3. Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology plos.io/45VTGBR

  4. Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology plos.io/45VTGBR

  5. Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology plos.io/45VTGBR

  6. Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology plos.io/45VTGBR

  7. Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology plos.io/45VTGBR

  8. What is the mechanistic link between the NLRP3 #inflammasome, #autophagy & inflammatory #bowel disease (IBD)? This study shows that VANGL2 reduces #IBD progression by recruiting the ubiquitin ligase MARCH8 to regulate NLRP3 activation via OPTN-mediated autophagy plosbiology plos.io/42FTqFO

  9. What is the mechanistic link between the NLRP3 #inflammasome, #autophagy & inflammatory #bowel disease (IBD)? This study shows that VANGL2 reduces #IBD progression by recruiting the ubiquitin ligase MARCH8 to regulate NLRP3 activation via OPTN-mediated autophagy plosbiology plos.io/42FTqFO

  10. What is the mechanistic link between the NLRP3 #inflammasome, #autophagy & inflammatory #bowel disease (IBD)? This study shows that VANGL2 reduces #IBD progression by recruiting the ubiquitin ligase MARCH8 to regulate NLRP3 activation via OPTN-mediated autophagy plosbiology plos.io/42FTqFO

  11. What is the mechanistic link between the NLRP3 #inflammasome, #autophagy & inflammatory #bowel disease (IBD)? This study shows that VANGL2 reduces #IBD progression by recruiting the ubiquitin ligase MARCH8 to regulate NLRP3 activation via OPTN-mediated autophagy plosbiology plos.io/42FTqFO

  12. What is the mechanistic link between the NLRP3 #inflammasome, #autophagy & inflammatory #bowel disease (IBD)? This study shows that VANGL2 reduces #IBD progression by recruiting the ubiquitin ligase MARCH8 to regulate NLRP3 activation via OPTN-mediated autophagy plosbiology plos.io/42FTqFO

  13. 'Here, we show that Arachidonic Acid inhibits the NLRP3 inflammasome, through a PLC-JNK-dependent mechanism, to supress IL-1β production under physiological conditions. This provides a mechanistic basis for how dietary manipulation such as fasting influences the inflammatory state and is likely to be critical for reducing the metaflammation underpinning many diseases induced by the Western Diet.'
    #Immunology #Inflammation #inflammasome #Metabolism

    cell.com/cell-reports/fulltext

  14. 'Here, we show that Arachidonic Acid inhibits the NLRP3 inflammasome, through a PLC-JNK-dependent mechanism, to supress IL-1β production under physiological conditions. This provides a mechanistic basis for how dietary manipulation such as fasting influences the inflammatory state and is likely to be critical for reducing the metaflammation underpinning many diseases induced by the Western Diet.'
    #Immunology #Inflammation #inflammasome #Metabolism

    cell.com/cell-reports/fulltext

  15. 'Here, we show that Arachidonic Acid inhibits the NLRP3 inflammasome, through a PLC-JNK-dependent mechanism, to supress IL-1β production under physiological conditions. This provides a mechanistic basis for how dietary manipulation such as fasting influences the inflammatory state and is likely to be critical for reducing the metaflammation underpinning many diseases induced by the Western Diet.'
    #Immunology #Inflammation #inflammasome #Metabolism

    cell.com/cell-reports/fulltext

  16. 'Here, we show that Arachidonic Acid inhibits the NLRP3 inflammasome, through a PLC-JNK-dependent mechanism, to supress IL-1β production under physiological conditions. This provides a mechanistic basis for how dietary manipulation such as fasting influences the inflammatory state and is likely to be critical for reducing the metaflammation underpinning many diseases induced by the Western Diet.'
    #Immunology #Inflammation #inflammasome #Metabolism

    cell.com/cell-reports/fulltext

  17. "Inflammasome-mediated caspase-1 activation facilitates innate immune control of Plasmodium in the liver, thereby limiting the incidence and severity of clinical malaria. However, caspase-1 processing occurs incompletely in both mouse and human hepatocytes and precludes the generation of mature IL-1β or IL-18, unlike in other cells. Why this is so or how it impacts Plasmodium control in the liver has remained unknown."
    #Malaria #inflammasome

    journals.aai.org/jimmunol/arti

  18. "Inflammasome-mediated caspase-1 activation facilitates innate immune control of Plasmodium in the liver, thereby limiting the incidence and severity of clinical malaria. However, caspase-1 processing occurs incompletely in both mouse and human hepatocytes and precludes the generation of mature IL-1β or IL-18, unlike in other cells. Why this is so or how it impacts Plasmodium control in the liver has remained unknown."
    #Malaria #inflammasome

    journals.aai.org/jimmunol/arti

  19. "Inflammasome-mediated caspase-1 activation facilitates innate immune control of Plasmodium in the liver, thereby limiting the incidence and severity of clinical malaria. However, caspase-1 processing occurs incompletely in both mouse and human hepatocytes and precludes the generation of mature IL-1β or IL-18, unlike in other cells. Why this is so or how it impacts Plasmodium control in the liver has remained unknown."
    #Malaria #inflammasome

    journals.aai.org/jimmunol/arti

  20. "Inflammasome-mediated caspase-1 activation facilitates innate immune control of Plasmodium in the liver, thereby limiting the incidence and severity of clinical malaria. However, caspase-1 processing occurs incompletely in both mouse and human hepatocytes and precludes the generation of mature IL-1β or IL-18, unlike in other cells. Why this is so or how it impacts Plasmodium control in the liver has remained unknown."
    #Malaria #inflammasome

    journals.aai.org/jimmunol/arti

  21. `Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

    nature.com/articles/s41467-023

  22. `Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

    nature.com/articles/s41467-023

  23. `Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

    nature.com/articles/s41467-023

  24. `Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

    nature.com/articles/s41467-023

  25. `Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

    nature.com/articles/s41467-023