We are analyzing https://link.springer.com/article/10.1007/s10753-020-01290-1.

Title:
A Spotlight on the Underlying Activation Mechanisms of the NLRP3 Inflammasome and its Role in Atherosclerosis: A Review | Inflammation
Description:
The world’s number one cause of death is cardiovascular diseases. The pathogenesis of different disease entities in the cardiovascular disease spectrum is complicated and multifactorial. Inflammation in these complicated etiologies serves as a key position and is a significant cause of atherosclerosis, which contributes to the underlying pathology. Therefore, therapeutic targeting of inflammatory pathways in patients with cardiovascular diseases such as atherosclerosis enhances cardiovascular results. Inflammasomes are intracellular protein complexes engaged in atherosclerosis pathogenesis and activated by multiple danger signals. Emerging proof has revealed that Nod-like receptor protein 3 (NLRP3) inflammasome, which regulates caspase-1 activation and later pro-interleukin processing, triggers inflammatory reactions in the vascular wall and leads to atherosclerotic plaque formation. Inflammasome-mediated signaling interference could decrease inflammation and mitigate illness severity. In this section, we provide an overview of the present literature on the underlying mechanisms leading to the activation of NLRP3 inflammasome and the role of NLRP3 inflammasome in the progression of atherogenesis and highlight the possibility of therapeutic interventions due to mechanisms involved in the of inhibition of NLRP3 activation.
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Keywords {🔍}

article, pubmed, google, scholar, cas, nlrp, inflammasome, activation, atherosclerosis, central, cell, inflammation, wang, inflammasomes, immunol, mechanisms, role, cardiovascular, caspase, access, nature, nat, biol, cholesterol, privacy, essential, cookies, content, signaling, fitzgerald, inhibits, efflux, yang, springer, chen, crystals, res, information, publish, search, underlying, review, liaqat, diseases, disease, vascular, atherogenesis, endothelial, bauernfeind, expression,

Topics {✒️}

sr/er–mitochondrial local communication month download article/chapter il-1β secretion clics-dependent chloride efflux suppressing ox-ldl uptake myocardial ischemia/reperfusion injury inflammasome-mediated signaling interference monocyte-endothelial cell interactions rna-binding protein tristetraprolin jak1/stat signaling pathway caspase-8 mediate priming article inflammation aims regulates caspase-1 activation full article pdf nitric oxide inhibits cardiovascular disease spectrum apoe-deficient mice crystal-induced activation privacy choices/manage cookies nicotine promotes atherosclerosis nlrp3 inflammasome activity caspase-1-sirtuin 1 pathway nlrp3 inflammasome activation pro-interleukin processing additional information publisher nlrp3 inflammasome expression atherosclerotic plaque formation ldlr−/− mice cxcl16/sr-psox nlrp3 activation downstream promoting cholesterol efflux hyperhomocysteinemia-aggravated inflammation reducing macrophage inflammation dna sensor aim2 stem cell proliferation related subjects nlrp3 inflammasome assembly article liaqat regulating nlrp3 expression noncanonical nlrp3 inflammasomes european economic area mitigate illness severity water influx activate proximal upstream event aluminum salts activate riphah international university authors declare global health burden nucleotide-binding domain underlying activation mechanisms

Questions {❓}

CXCL16/SR-PSOX-A friend or a foe in atherosclerosis?
The NLRP3 inflammasome: A sensor for metabolic danger?
What do we know about the inflammasome in humans?

Schema {🗺️}

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