NFAT5 Mediates Hypertonic Stress-Induced Atherosclerosis via Activating NLRP3 Inflammasome in Endothelium
August 2019
in “
Cell Communication and Signaling
”
TLDR NFAT5 triggers atherosclerosis under stress by activating inflammation in blood vessels.
The study investigated the role of NFAT5 in high-salt-induced atherosclerosis using ApoE−/− mice and cultured endothelial cells. It found that high-salt intake promoted atherosclerosis by inducing NFAT5, which activated the NLRP3 inflammasome and increased IL-1β secretion in endothelial cells, partly mediated by reactive oxygen species (ROS). NFAT5 directly bound to the promoter regions of NLRP3 and IL-1β, playing a crucial role in early activation of NLRP3-inflammasome-mediated endothelium innate immunity. The study suggested that targeting NFAT5 could be a promising strategy for treating atherosclerosis.