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组织型纤溶酶原激活剂介导的血小板衍生生长因子信号传导与中风中的神经血管耦合

Tissue plasminogen activator-mediated PDGF signaling and neurovascular coupling in stroke.

作者信息

Su E J, Fredriksson L, Schielke G P, Eriksson U, Lawrence D A

机构信息

Department of Internal Medicine, University of Michigan Medical School, MI 48109, USA.

出版信息

J Thromb Haemost. 2009 Jul;7 Suppl 1(Suppl 1):155-8. doi: 10.1111/j.1538-7836.2009.03402.x.

DOI:10.1111/j.1538-7836.2009.03402.x
PMID:19630790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2912222/
Abstract

The use of tissue plasminogen activator (tPA) as a thrombolytic treatment in ischemic stroke is limited largely due to concerns for hemorrhagic complications. The underlying mechanisms are still unknown, but evidence is beginning to emerge that tPA interacts with key regulators of the neurovascular unit (NVU), and that these interactions may contribute to the undesirable side effects associated with the use of tPA in ischemic stroke. Understanding these connections and tPA's normal function within the NVU may offer new insights into future therapeutic approaches.

摘要

组织型纤溶酶原激活剂(tPA)在缺血性卒中中作为溶栓治疗的应用受到很大限制,主要是因为担心出血并发症。其潜在机制尚不清楚,但已有证据表明,tPA与神经血管单元(NVU)的关键调节因子相互作用,而这些相互作用可能导致tPA在缺血性卒中应用中出现不良副作用。了解这些联系以及tPA在NVU中的正常功能,可能为未来的治疗方法提供新的见解。

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Activation of PDGF-CC by tissue plasminogen activator impairs blood-brain barrier integrity during ischemic stroke.组织型纤溶酶原激活剂激活血小板衍生生长因子CC会损害缺血性中风期间的血脑屏障完整性。
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