传出细胞增多
CD36
医学
冲程(发动机)
黑质
神经保护
缺血
单核细胞
内科学
内分泌学
生物
巨噬细胞
多巴胺
多巴胺能
受体
体外
工程类
机械工程
生物化学
作者
Hyunwoo Ju,Il‐Doo Kim,Ina Pavlova,Shang Mu,Keun Woo Park,Joseph Minkler,Ahmed Madkoor,Wei Wang,Xiaoman Wang,Zhuhao Wu,Jiwon Yang,Maria Febbraio,John W. Cave,Sunghee Cho
标识
DOI:10.1161/circresaha.124.325428
摘要
RIC induces a shift in monocytes to a proinflammatory state with elevated CD36 levels, and this is associated with CD36-dependent efferocytosis in Mφs that rescues delayed transneuronal degeneration in the postischemic brain and promotes stroke recovery. Together, these findings provide novel insight into our mechanistic understanding of how RIC improves poststroke recovery.
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