Guo Pingping, Li Hongmin, Zhang Xiangyu, Liu Yang, Xue Sara, Yong Voon Wee, Xue Mengzhou
Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.
Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB T2N 4N1, Canada.
Mol Med Rep. 2025 Aug;32(2). doi: 10.3892/mmr.2025.13590. Epub 2025 Jun 6.
Hemorrhagic transformation (HT) is a devasting complication following acute ischemic stroke with high morbidity and mortality. The pathogenesis of HT mainly involves ischemia‑reperfusion‑induced oxidative stress, neuroinflammation, thrombolytic therapy‑associated toxicity and, most critically, blood‑brain barrier (BBB) disruption. Matrix metalloproteinase‑9 (MMP‑9) serves as a critical mediator of HT through degrading extracellular matrix components and disrupting tight junction proteins, thereby compromising BBB integrity. Thus, elaborating the underlying molecular mechanisms of MMP‑9 in destroying BBB and promoting HT is essential to improve the outcome of ischemic stroke patients. Furthermore, to provide beneficial insights for the treatment of ischemic stroke, precise understanding of the potential role of MMP‑9 as a biomarker and treatment target to predict and ameliorate the risk of HT is also necessary.
出血性转化（HT）是急性缺血性卒中后一种严重的并发症，具有高发病率和死亡率。HT的发病机制主要涉及缺血再灌注诱导的氧化应激、神经炎症、溶栓治疗相关毒性，最关键的是血脑屏障（BBB）破坏。基质金属蛋白酶-9（MMP-9）通过降解细胞外基质成分和破坏紧密连接蛋白，从而损害BBB完整性，成为HT的关键介质。因此，阐明MMP-9破坏BBB和促进HT的潜在分子机制对于改善缺血性卒中患者的预后至关重要。此外，为了为缺血性卒中的治疗提供有益的见解，准确了解MMP-9作为预测和改善HT风险的生物标志物和治疗靶点的潜在作用也是必要的。
