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REVIEW article
Front. Neurosci.
Sec. Neurogenesis
Volume 19 - 2025 | doi: 10.3389/fnins.2025.1536055
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Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process faced by brain tissues after ischemic stroke treatment, which involves mechanisms of inflammatory response, oxidative stress and apoptosis, and severely affects treatment outcome. Lipocalin-2 (LCN2), an acute-phase protein, is significantly up-regulated after CIRI and promotes neural repair by enhancing astrocyte phagocytosis, but its over-activation may also trigger secondary inflammation and demyelination injury. LCN2 also plays a key role in neuroinflammation regulation by regulating the polarization state of astrocytes and the release of inflammatory factors, and may affect the integrity of the blood-brain barrier and a variety of pathologic injury processes. In view of the important role of LCN2 in CIRI, this article reviews the mechanism of LCN2, aiming to provide new ideas and methods for the treatment of ischemic stroke.
Keywords: Cerebral ischemia-reperfusion injury, Lipocalin-2, Inflammatory Response, astrocyte, Apoptosis
Received: 28 Nov 2024; Accepted: 10 Mar 2025.
Copyright: © 2025 Cai, Yuan, Huang, Zhang, Zou and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Xiao-Ming Zhang, Hubei University of Chinese Medicine, Wuhan, 430065, Hubei Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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