Abstract
nectin inhibited these outcomes. Compared to monocytes from Adipoq+/+ mice, those from Adipoq-/littermates showed a w6-fold greater production of MPs (Cd11b+/ Ly6Chi/AnnexinV+) following LPS stimulation. CONCLUSION: We report a novel mechanism through which mono-MPs sustain NLRP3 inflammasome activation and endothelial dysfunction. These data reveal a previously unknown atheroprotective mechanism for adiponectin that may account for the inverse association observed between circulating adiponectin levels and the risk of diabetes and obesity.
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