The Plasminogen Activation System Promotes Neurorepair in the Ischemic Brain

التفاصيل البيبلوغرافية
العنوان: The Plasminogen Activation System Promotes Neurorepair in the Ischemic Brain
المؤلفون: Manuel Yepes
المصدر: Current Drug Targets
بيانات النشر: Bentham Science Publishers, 2019.
سنة النشر: 2019
مصطلحات موضوعية: 0301 basic medicine, Plasmin, Clinical Biochemistry, Central nervous system, Ischemia, Neuroprotection, Fibrin, Article, cerebral ischemia, Brain Ischemia, Receptors, Urokinase Plasminogen Activator, Synapse, 03 medical and health sciences, 0302 clinical medicine, Drug Discovery, medicine, Animals, Humans, neurorepair, plasmin, Pharmacology, biology, urokinase-type plasminogen activator, business.industry, Tissue-type plasminogen activator, medicine.disease, Urokinase receptor, 030104 developmental biology, medicine.anatomical_structure, Gene Expression Regulation, Tissue Plasminogen Activator, Cancer research, biology.protein, Molecular Medicine, neuroprotection, business, Plasminogen activator, 030217 neurology & neurosurgery, medicine.drug
الوصف: The plasminogen activation (PA) system was originally thought to exclusively promote the degradation of fibrin by catalyzing the conversion of plasminogen into plasmin via two serine proteinases: tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). However, experimental evidence accumulated over the last 30 years indicates that tPA and uPA are also found in the central nervous system (CNS), where they have a plethora of functions that not always require plasmin generation or fibrin degradation. For example, plasminogen-dependent and - independent effects of tPA and uPA play a central role in the pathophysiological events that underlie one of the leading causes of mortality and disability in the world: cerebral ischemia. Indeed, recent work indicates that while the rapid release of tPA from the presynaptic compartment following the onset of cerebral ischemia protects the synapse from the deleterious effects of the ischemic injury, the secretion of uPA and its binding to its receptor (uPAR) during the recovery phase promotes the repair of synapses that have been lost to the acute ischemic insult. This restorative role of uPA has high translational significance because to this date there is no effective approach to induce neurorepair in the ischemic brain. Here we will discuss recent evidence that bridges the gap between basic research in the field of the PA system and the bedside of ischemic stroke patients, indicating that uPA and uPAR are potential targets for the development of therapeutic strategies to promote neurological recovery among ischemic stroke survivors.
اللغة: English
تدمد: 1873-5592
1389-4501
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4413bcf21862b10e46c7452b6d4db615Test
http://europepmc.org/articles/PMC6700753Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....4413bcf21862b10e46c7452b6d4db615
قاعدة البيانات: OpenAIRE
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