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10.1038/aps.2011.60 http://scihub22266oqcxt.onion/10.1038/aps.2011.60 C4009967!4009967!21552293     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Pharmacol+Sin 2011 ; 32 (6): 725-33 Nephropedia Template TP {{tp|p=21552293|t=2011. TRPM7 in cerebral ischemia and potential target for drug development in stroke |pdf=|usr=}}{{21552293}} gab.com Text TRPM7 in cerebral ischemia and potential target for drug development in stroke JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=21552293 #FOAvip Searching for effective pharmacological agents for stroke treatment has largely been unsuccessful. Despite initial excitement, antagonists for glutamate receptors, the most studied receptor channels in ischemic stroke, have shown insufficient neuroprotective effects in clinical trials. Outside the traditional glutamate-mediated excitotoxicity, recent evidence suggests few non-glutamate mechanisms, which may also cause ionic imbalance and cell death in cerebral ischemia. Transient receptor potential melastatin 7 (TRPM7) is a Ca2+ permeable, non-selective cation channel that has recently gained attention as a potential cation influx pathway involved in ischemic events. Compelling new evidence from an in vivo study demonstrated that suppression of TRPM7 channels in adult rat brain in vivo using virally mediated gene silencing approach reduced delayed neuronal cell death and preserved neuronal functions in global cerebral ischemia. In this review, we will discuss the current understanding of the role of TRPM7 channels in physiology and pathophysiology as well as its therapeutic potential in stroke. Twit Text FOAVip TRPM7 in cerebral ischemia and potential target for drug development in stroke ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=21552293 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21552293 #FOAvip English Wikipedia <ref>{{Cite pmid|21552293}}</ref> TRPM7 in cerebral ischemia and potential target for drug development in stroke #MMPMID21552293 Bae CYj; Sun Hs Acta Pharmacol Sin 2011[Jun]; 32 (6): 725-33 PMID21552293show ga Searching for effective pharmacological agents for stroke treatment has largely been unsuccessful. Despite initial excitement, antagonists for glutamate receptors, the most studied receptor channels in ischemic stroke, have shown insufficient neuroprotective effects in clinical trials. Outside the traditional glutamate-mediated excitotoxicity, recent evidence suggests few non-glutamate mechanisms, which may also cause ionic imbalance and cell death in cerebral ischemia. Transient receptor potential melastatin 7 (TRPM7) is a Ca2+ permeable, non-selective cation channel that has recently gained attention as a potential cation influx pathway involved in ischemic events. Compelling new evidence from an in vivo study demonstrated that suppression of TRPM7 channels in adult rat brain in vivo using virally mediated gene silencing approach reduced delayed neuronal cell death and preserved neuronal functions in global cerebral ischemia. In this review, we will discuss the current understanding of the role of TRPM7 channels in physiology and pathophysiology as well as its therapeutic potential in stroke. äTRPM7 in cerebral ischemia and potential target for drug development i(epmc).pdf DeepDyve Pubget Overpricing