Abstract
Intracerebral hemorrhagic transformation (HT) is well recognized as a common cause of hemorrhage in patients with ischemic stroke. HT after acute ischemic stroke contributes to early mortality and adversely affects functional recovery. The risk of HT is especially high when patients receive thrombolytic reperfusion therapy with tissue plasminogen activator, the only available treatment for ischemic stroke. Although many important publications address preclinical models of ischemic stroke, there are no current recommendations regarding the conduct of research aimed at understanding the mechanisms and prediction of HT. In this review, we discuss the underlying mechanisms for HT after ischemic stroke, provide an overview of the models commonly used for the study of HT, and discuss biomarkers that might be used for the early detection of this challenging clinical problem.
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Acknowledgments
This work was supported by grants from the National Natural Science Foundation of China (81171112, 81371272 to M.C.L., 81372683 to Q.X.C.) and grants from NIH (K01AG031926, R01NS078026, R01AT007317 to J. W.). We thank Claire Levine, MS, ELS, for the assistance with manuscript preparation.
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Wei Wang and Mingchang Li contributed equally to the manuscript.
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Wang, W., Li, M., Chen, Q. et al. Hemorrhagic Transformation after Tissue Plasminogen Activator Reperfusion Therapy for Ischemic Stroke: Mechanisms, Models, and Biomarkers. Mol Neurobiol 52, 1572–1579 (2015). https://doi.org/10.1007/s12035-014-8952-x
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DOI: https://doi.org/10.1007/s12035-014-8952-x