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Endothelial CCRL2 induced by disturbed flow promotes atherosclerosis via chemerin-dependent β2 integrin activation in monocytes.

Chaojun TangGuona ChenFan WuYiren CaoFei YangTao YouChu LiuMenglu LiShuhong HuLijie RenQiongyu LuWei DengYing XuGuixue WangHanjoong JoYonghong ZhangYi WuBrian A ZabelLi Zhu
Published in: Cardiovascular research (2023)
Our findings indicate that d-flow-induced CCRL2 promotes atherosclerotic plaque formation via a novel CCRL2-chemerin-β2 integrin axis, providing potential targets for the prevention or therapeutic intervention of atherosclerosis.
Keyphrases
  • cardiovascular disease
  • randomized controlled trial
  • high glucose
  • endothelial cells
  • coronary artery disease
  • cell adhesion
  • diabetic rats
  • type diabetes
  • dendritic cells
  • oxidative stress
  • risk assessment