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Title[redir]:
Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome - PMC
Description:
The interleukin-1 (IL-1) family of cytokines has been implicated in the pathogenesis of atherosclerosis in previous studies. The NLRP3 inflammasome has recently emerged as a pivotal regulator of IL-1β maturation and secretion by macrophages. Little ...
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Keywords {🔍}
mice, atherosclerosis, doi, nlrp, apoe, inflammasome, plaque, pubmed, google, scholar, macrophages, ilβ, progression, asc, pmc, caspase, mouse, model, plaques, atherosclerotic, role, nlm, cell, interleukin, figure, cells, pathogenesis, highfat, diet, ilα, cholesterol, bone, receptor, nature, ncbi, search, article, studies, stability, results, inflammation, staining, study, cytokines, phenotype, differences, genotypes, disease, shown, inflammasomes,
Topics {✒️}
100 ng/ml ultra-pure lipopolysaccharide bone marrow-derived cells il-1α/β-deficient cells cytoplasmic pattern-recognition receptors apolipoprotein e-deficient mice il-1α-deficient apoe−/− mice il-1β-deficient apoe−/− mice naturally-occurring endogenous antagonist pmc beta search interleukin-1alpha gene expression obtain double-deficient mice related parent il-1α low-density lipoprotein receptor oxidized low-density lipoproteins smooth muscle actin similar high-fat diet nlrp3 inflammasome-deficient macrophages murine primary macrophages nlrp3 inflammasome-dependent manner atherosclerotic plaque-infiltrating macrophages publisher site pdf interleukin-1 receptor antagonist release active il-1β md-phd grant van der hoorn il-1 receptor antagonist double-knockout mice endogenous danger signals active il-1α control apoe−/− group license information pmcid total lesion size atherosclerotic plaque area anti-inflammatory agents murine apolipoprotein mature active form plaque-infiltrating macrophages high-fat diet double-edged sword apoe−/− mice resulted mol cell biol united states government pmc disclaimer remains incompletely understood attracted considerable attention anti-mac-2 staining coronary artery stenosis thinned fibrous cap genes possibly contributing genetically induced overexpression
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