从γ-原钙黏蛋白中挽救KLF2/4以减轻血管炎症和动脉粥样硬化。
Saving KLF2/4 from γ-protocadherin to reduce vascular inflammation and atherosclerosis.
作者信息
Park Christian, Baek Kyung In, Jo Hanjoong
机构信息
Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.
出版信息
Nat Cardiovasc Res. 2024 Sep;3(9):1021-1023. doi: 10.1038/s44161-024-00523-y.
Atherosclerosis occurs in arterial regions exposed to disturbed flow, where endothelial expression of flow-sensitive, atheroprotective genes such as and is reduced. Protecting the endothelial expression of KLF2 and KLF4 from inhibitory factors could be a therapeutic approach to prevent vascular inflammation and atherosclerosis.
动脉粥样硬化发生在血流紊乱的动脉区域，在此处，血流敏感的抗动脉粥样硬化基因（如 和 ）的内皮表达会降低。保护KLF2和KLF4的内皮表达免受抑制因子影响可能是预防血管炎症和动脉粥样硬化的一种治疗方法。
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