Inflammasome-Independent NALP3 Contributes to High-Salt Induced Endothelial Dysfunction.

ABSTRACT: Backgrounds and Aims: Na⁺ is an important nutrient and its intake, mainly from salt (NaCl), is essential for normal physiological function. However, high salt intake may lead to vascular injury, independent of a rise in blood pressure (BP). Canonical NALP3 inflammasome activation is a caspase-1 medicated process, resulting in the secretion of IL-18 and IL-1β which lead to endothelial dysfunction. However, some researches uncovered a direct and inflammasome-independent role of NALP3 in renal injury. Thus, this study was designed to investigate the possible mechanisms of NALP3 in high salt induced endothelial dysfunction. Methods and Results: Changes in endothelial function were measured by investigating mice (C57BL/6J, NALP3^-/- and wild-type, WT) fed with

SUBMITTER: Fu H 

PROVIDER: S-EPMC6113916 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature