Scholarlink

<p>Intracerebral hemorrhage (ICH) is a severe stroke subtype characterized by high mortality and disability rates. Secondary brain injury is a critical determinant of prognosis, yet effective interventions remain limited. Lipocalin-2 (LCN2), as an acute-phase protein, plays a complex and context-dependent multifaceted role in the pathophysiological processes following ICH. Substantial evidence indicates that LCN2 exacerbates secondary brain injury through multiple mechanisms, including driving neuroinflammation, disrupting the blood-brain barrier, participating in oxidative stress, inducing programmed cell death, and impairing neuroplasticity. Meanwhile, some studies suggest that under specific conditions, LCN2 may also influence the repair process by mechanisms such as limiting excessive inflammatory responses and modulating glial cell functions. Furthermore, the dynamic expression profile of LCN2 positions it as a potential biomarker for assessing ICH risk factors such as hypertension, atherosclerosis, and insulin resistance. Additionally, both pharmacological agents targeting LCN2 and emerging nanotherapeutic strategies have shown promising application prospects. This review aims to comprehensively elucidate the pivotal role of LCN2 in the pathogenesis and progression of ICH, its potential as a biomarker, and its prospects as a therapeutic target, thereby providing new theoretical foundations and directions for the precise prevention and treatment of ICH.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting

  • 期刊论文

  • 发表日期：

    2026年3月10日

查看全文
  • Yue Sun,
  • Wentao Sun,
  • Lei Zheng,
  • Baiwen Zhang,
  • Jiawei Liu,
  • Wei Zou

摘要

Intracerebral hemorrhage (ICH) is a severe stroke subtype characterized by high mortality and disability rates. Secondary brain injury is a critical determinant of prognosis, yet effective interventions remain limited. Lipocalin-2 (LCN2), as an acute-phase protein, plays a complex and context-dependent multifaceted role in the pathophysiological processes following ICH. Substantial evidence indicates that LCN2 exacerbates secondary brain injury through multiple mechanisms, including driving neuroinflammation, disrupting the blood-brain barrier, participating in oxidative stress, inducing programmed cell death, and impairing neuroplasticity. Meanwhile, some studies suggest that under specific conditions, LCN2 may also influence the repair process by mechanisms such as limiting excessive inflammatory responses and modulating glial cell functions. Furthermore, the dynamic expression profile of LCN2 positions it as a potential biomarker for assessing ICH risk factors such as hypertension, atherosclerosis, and insulin resistance. Additionally, both pharmacological agents targeting LCN2 and emerging nanotherapeutic strategies have shown promising application prospects. This review aims to comprehensively elucidate the pivotal role of LCN2 in the pathogenesis and progression of ICH, its potential as a biomarker, and its prospects as a therapeutic target, thereby providing new theoretical foundations and directions for the precise prevention and treatment of ICH.