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Inhibiting sEH suppresses NF-κB p65 signaling and reduces CXCL10 expression as a potential therapeutic target in HT.

Jing FengXianghong XuWei CaiXingwen YangRuilan NiuZiqi HanLimin Tian
Published in: The Journal of clinical endocrinology and metabolism (2024)
Our findings suggest that sEH/NF-κB p65/CXCL10-CXCR3 might be promising therapeutic targets for HT.
Keyphrases
  • signaling pathway
  • pi k akt
  • lps induced
  • poor prognosis
  • nuclear factor
  • oxidative stress
  • inflammatory response
  • cell proliferation
  • binding protein
  • long non coding rna
  • toll like receptor
  • climate change
  • cell migration