title: TRPM7 and ischemic CNS injury.
abstract: Ischemic brain damage represents a major source of morbidity and mortality in westernized society and poses a significant financial burden on the health care system. To date, few effective therapies have been realized to treat stroke and once promising avenues such as antiexcitotoxic therapy with NMDA receptor antagonists have not proven clinically useful. Thus, we need to identify new targets for research and therapeutic intervention of the neurodegeneration caused by stroke. Transient receptor potential (TRP) channels are an exciting new family of cation channels that respond to intracellular and extracellular stimuli. Indeed, several members can be induced by oxidative stress and oxygen free radicals. We have recently demonstrated that one member, TRPM7, is an essential mediator of anoxic neuronal death that is activated by oxidative stress, in parallel to excitotoxic signal pathways. Thus, future treatment of ischemic brain injury may need to include strategies that inhibit or modulate TRPM7 activity. Further investigation of the physiology and pathophysiology of TRPM7 and other TRP family members is needed to provide both pharmacological targets and a better understanding of ischemic brain disorders.
authors.affiliation: Applied and Interventional Research and Division of Neurosurgery, Toronto Western Research Institute, 399 BathurstStreet, Toronto, Ontario M5T 2S8, Canada.
authors.forename: Michelle M
authors.initials: MM
authors.lastname: Aarts
authors.forename: Michael
authors.initials: M
authors.lastname: Tymianski
mesh_terms: D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology; D007473:Ion Channels / Q000737:chemistry / Q000378:metabolism*; D008565:Membrane Proteins / Q000737:chemistry / Q000378:metabolism*; D011494:Protein Kinases / Q000737:chemistry / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D007473:Ion Channels; D008565:Membrane Proteins; D011494:Protein Kinases