Further characterization of the lesion phenotype showed that 90% (9/10) of lesions in ApoE−/− Nur77−/− group and 40% (4/10) of lesions in ApoE−/− group had vulnerable features, accompanied by an increasing trend of multiple layers with discontinuity (70% vs. 30%), indicative of plaque instability ( Table 1 ).
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Nur77 Deficiency Exacerbates Macrophage NLRP3 Inflammasome-Mediated Inflammation and Accelerates Atherosclerosis.
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