创伤性脑损伤
冲程(发动机)
血脑屏障
脂质运载蛋白
神经科学
脑损伤
医学
生物信息学
炎症
促炎细胞因子
免疫学
内科学
生物
中枢神经系统
工程类
精神科
机械工程
作者
Korsin Laohavisudhi,Sirawit Sriwichaiin,Tanawat Attachaipanich,Borwon Wittayachamnankul,Nipon Chattipakorn,Siriporn C. Chattipakorn
标识
DOI:10.1016/j.expneurol.2024.114885
摘要
Brain injuries, including strokes and traumatic brain injuries (TBI), are a major global health concern, contributing significantly to both mortality and long-term disability. Recent research has identified lipocalin-2 (LCN2), a glycoprotein secreted by various brain cells, as a key factor in influencing brain injury outcomes. Evidence from animal and clinical studies firmly establishes the pivotal role of LCN2 in driving the inflammatory responses triggered by damage to brain tissue. Furthermore, increased LCN2 promotes cellular differentiation, blood-brain barrier breakdown, and decreases cell viability. Interventions with LCN2 inhibitors attenuated brain injury through a reduction in the inflammation process and enhanced cellular viability. Potential mechanisms of LCN2 involve several pathways including the Janus kinase-2 (JAK2)-signal transducers and the transcription-3 (STAT3) signaling, hypoxia-inducible factor 1-alpha (HIF-1α)-LCN2-vascular endothelial growth factor alpha (VEGFα), and the PKR-like ER kinase (PERK) pathways. LCN2 itself interacts with diverse inflammatory cytokines in TBI and intracranial hemorrhage (ICH), resulting in disruption of the blood-brain barrier, increased programmed cell death, and an imbalance in iron homeostasis. Clinical studies have also shown that increased LCN2 level can act as a prognostic biomarker of outcomes following brain injuries. Therefore, this review aims to comprehensively evaluate the role and underlying mechanisms of LCN2 in brain injuries, including stroke and TBI, and explore potential therapeutic interventions targeting LCN2 in these conditions.
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