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10.1038/aps.2012.94

http://scihub22266oqcxt.onion/10.1038/aps.2012.94
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22820907!4086489!22820907
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suck abstract from ncbi

pmid22820907      Acta+Pharmacol+Sin 2013 ; 34 (1): 10-6
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  • Current understanding of TRPM7 pharmacology and drug development for stroke #MMPMID22820907
  • Bae CY; Sun HS
  • Acta Pharmacol Sin 2013[Jan]; 34 (1): 10-6 PMID22820907show ga
  • The initial excitement and countless efforts to find a pharmacological agent that disrupts the excitotoxic pathway of ischemic neuronal death have only led to disappointing clinical trials. Currently, a thrombolytic agent called recombinant tissue plasminogen activator (rt-PA) is the only pharmacological treatment available for patients with acute ischemic stroke in most countries. Even though its efficacy has been confirmed repeatedly, rt-PA is considerably underused due to reasons including a short therapeutic window and repeated complications associated with its use. A search for alternative mechanisms that may operate dependently or independently with the well-established excitotoxic mechanism has led researchers to the discovery of newly described non-glutamate mechanisms. Among the latter, transient receptor potential melastatin 7 (TRPM7) is one of the important nonglutamate mechanisms in stroke, which has been evaluated in both in-vitro and in-vivo. In this review, we will discuss the current state of pharmacological treatments of ischemic stroke and provide evidence that TRPM7 is a promising therapeutic target of stroke.
  • |Animals[MESH]
  • |Drug Discovery/methods[MESH]
  • |Fibrinolytic Agents/therapeutic use[MESH]
  • |Humans[MESH]
  • |Molecular Targeted Therapy/*methods[MESH]
  • |Neuroprotective Agents/therapeutic use[MESH]
  • |Protein Serine-Threonine Kinases[MESH]
  • |Receptors, Glutamate/metabolism[MESH]
  • |Recombinant Proteins/therapeutic use[MESH]
  • |Stroke/*drug therapy/metabolism[MESH]
  • |TRPM Cation Channels/*antagonists & inhibitors/*metabolism[MESH]
  • |Thrombolytic Therapy/methods[MESH]


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