NFAT5 Mediates Hypertonic Stress-Induced Atherosclerosis via Activating NLRP3 Inflammasome in Endothelium

    August 2019 in “ Cell Communication and Signaling
    Pingping Ma, Shenfang Zha, Xinkun Shen, Yulan Zhao, Li Li, Li Yang, Mingxing Lei, Wanqian Liu
    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.
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