Key result
Hydroxytyrosol acetate reduces vascular endothelial inflammation via the TNFRSF1A/SIRT6/PKM2 pathway in preclinical models.
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Demonstrates that hydroxytyrosol acetate suppresses vascular inflammation via TNFRSF1A and SIRT6-PKM2 signaling, suggesting therapeutic value for endothelial protection.
abolished the inhibition of inflammatory response by HT-AC in the thoracic aorta of hypercholesterolemic mice. In vitro study also showed that knockdown of SIRT6 reduced the inhibition of inflammatory response by HT-AC, whereas overexpression of SIRT6 augmented the inhibition of inflammatory response by HT-AC in HUVECs. Further study demonstrated that HT-AC exerts its anti-inflammatory effect partly via the SIRT6-mediated PKM2 signaling pathway. In addition, HT-AC inhibited TNF-induced inflammatory response through the TNF receptor superfamily member 1A (TNFRSF1A) signaling pathway. These findings indicate that HT-AC regulates the vascular endothelial inflammatory response partly through the TNFRSF1A/SIRT6/PKM2-mediated signaling pathway.
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Yao et al. (2019) studied Vascular endothelial inflammation / hypercholesterolemia. Hydroxytyrosol acetate (HT-AC) was evaluated on Vascular endothelial inflammatory response. Hydroxytyrosol acetate (HT-AC) inhibits vascular endothelial inflammation in hypercholesterolemic mice and HUVECs partly via the TNFRSF1A/SIRT6/PKM2 signaling pathway.
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