Microglia and bradykinin cross talk in poststroke cognitive impairment in diabetes

被引:8
作者
Baric, Anja [1 ]
Radmilovic, Marina Dobrivojevic [1 ]
机构
[1] Univ Zagreb, Croatian Inst Brain Res, Dept Histol & Embryol, Sch Med, Zagreb, Croatia
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2021年 / 320卷 / 06期
关键词
bradykinin; diabetes mellitus; microglia; poststroke cognitive impairment; ISCHEMIA-REPERFUSION INJURY; NITRIC-OXIDE; RECEPTORS; STROKE; EXPRESSION; DEFICITS; RELEASE; DECLINE; KININS; TISSUE;
D O I
10.1152/ajpcell.00402.2020
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Stroke is one of the leading causes of mortality and the leading cause of long-term disability worldwide. Although cognitive impairment is a common consequence of stroke, the underlying pathophysiological processes that lead to it are still poorly understood. Recently, more studies have shown evidence of the involvement of diabetes in producing a chronic neuroinflammatory state, which ultimately alters the recovery of function and cognition after stroke. To better understand the impact of diabetes on poststroke recovery, here we highlight the recent insights on the role of diabetes in neuroinflammation, especially regarding its effect on microglial function, and the emerging data on the involvement of kinins in both diabetes and neuroinflammation.
引用
收藏
页码:C613 / C618
页数:6
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