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Matrix metalloproteinase‑9 in hemorrhagic transformation after acute ischemic stroke (Review)
Pingping Guo1, Hongmin Li1, Xiangyu Zhang1
1Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.
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.
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.

