Journal
FRONTIERS IN MOLECULAR NEUROSCIENCE
Volume 15, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2022.930526
Keywords
LCN2; neuroinflammation; ischemic stroke; intracerebral hemorrhage; intraventricular hemorrhage; subarachnoid hemorrhage
Categories
Funding
- National Natural Science Foundation of China
- Natural Science Foundation of Hunan Province
- Hunan Provincial Health and Health Committee Foundation of China
- Xiangya Hospital Central South University Postdoctoral Foundation
- Fundamental Research Funds for the Central Universities of Central South University
- [82073893]
- [2022JJ30943]
- [2022JJ20095]
- [202204044869]
- [2021zzts1027]
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Ischemic and hemorrhagic stroke are the leading causes of disability and death globally. Lipocalin 2 (LCN2) plays a vital role in brain injury after stroke, but its specific mechanism and involvement of primary receptors remain unclear. Further research is needed to explore LCN2-induced brain damage and identify therapeutic targets.
Ischemic and hemorrhagic stroke (including intracerebral hemorrhage, intraventricular hemorrhage, and subarachnoid hemorrhage) is the dominating cause of disability and death worldwide. Neuroinflammation, blood-brain barrier (BBB) disruption, neuronal death are the main pathological progress, which eventually causes brain injury. Increasing evidence indicated that lipocalin 2 (LCN2), a 25k-Da acute phase protein from the lipocalin superfamily, significantly increased immediately after the stroke and played a vital role in these events. Meanwhile, there exists a close relationship between LCN2 levels and the worse clinical outcome of patients with stroke. Further research revealed that LCN2 elimination is associated with reduced immune infiltrates, infarct volume, brain edema, BBB leakage, neuronal death, and neurological deficits. However, some studies revealed that LCN2 might also act as a beneficial factor in ischemic stroke. Nevertheless, the specific mechanism of LCN2 and its primary receptors (24p3R and megalin) involving in brain injury remains unclear. Therefore, it is necessary to investigate the mechanism of LCN2 induced brain damage after stroke. This review focuses on the role of LCN2 and its receptors in brain injury and aiming to find out possible therapeutic targets to reduce brain damage following stroke.
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