Lipocalin-2 and Cerebral Stroke

被引:13
|
作者
Luo, Chao [1 ]
Zhou, Shuai [1 ,2 ]
Yin, Shi [1 ]
Jian, Lipeng [1 ]
Luo, Pengren [1 ]
Dong, Jigeng [1 ]
Liu, Erheng [1 ]
机构
[1] Kunming Univ Sci & Technol, Dept Neurosurg, Affiliated Hosp, Kunming, Peoples R China
[2] First Peoples Hosp Yunnan Prov, Dept Neurosurg, Kunming, Peoples R China
来源
基金
中国国家自然科学基金;
关键词
cerebral stroke; lipocalin-2 (LCN-2); blood brain barrier; central nervous system; secondary injury; iron dysregulation; neurovascular unit (NVU); BLOOD-BRAIN-BARRIER; INTRACEREBRAL HEMORRHAGE; OXIDATIVE STRESS; UP-REGULATION; WHITE-MATTER; CELL-DEATH; INFLAMMATORY ACTIVATION; NEUROVASCULAR UNIT; IRON HOMEOSTASIS; ISCHEMIC-STROKE;
D O I
10.3389/fnmol.2022.850849
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Stroke is a common and devastating disease with an escalating prevalence worldwide. The known secondary injuries after stroke include cell death, neuroinflammation, blood-brain barrier disruption, oxidative stress, iron dysregulation, and neurovascular unit dysfunction. Lipocalin-2 (LCN-2) is a neutrophil gelatinase-associated protein that influences diverse cellular processes during a stroke. The role of LCN-2 has been widely recognized in the peripheral system; however, recent findings have revealed that there are links between LCN-2 and secondary injury and diseases in the central nervous system. Novel roles of LCN-2 in neurons, microglia, astrocytes, and endothelial cells have also been demonstrated. Here, we review the evidence on the regulatory roles of LCN-2 in secondary injuries following a stroke from various perspectives and the pathological mechanisms involved in the modulation of stroke. Overall, our review suggests that LCN-2 is a promising target to promote a better understanding of the neuropathology of stroke.
引用
收藏
页数:9
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