Are the transient receptor potential melastatin (TRPM) channels important in magnesium homeostasis following traumatic brain injury?
Traumatic brain injury (TBI) confers a major burden to Western society and effective treatments are urgently required to improve the long-term deficits that inflict TBI survivors. Depletion of intracellular Mg(2+) is a well-known phenomenon occurring after TBI and is associated with poor neurological outcome. However, despite success in pre-clinical experimental studies, therapies utilizing Mg(2+) have not always proven to be clinically effective. Recent evidence implicates members of the transient receptor potential melastatin (TRPM) channel family in processes leading to neuronal cell death following ischemic injury, however, the exact mechanism by which this occurs is not completely understood. Specifically, TRPM7 and TRPM6 are two channels that have been identified as potentially playing a role in regulating Mg(2+) homeostasis, although whether this role in magnesium regulation and neuronal injury is significant is controversial. The purpose of this review is to explore the relationship between TRPM family members and Mg(2+) homeostasis, including their potential involvement in secondary injury processes leading to cell death following TBI.
Discipline of Pathology, School of Medical Sciences, The University of Adelaide, Australia.
Naomi L
NL
Cook
Corinna
C
Van Den Heuvel
Robert
R
Vink
D001930:Brain Injuries / Q000401:mortality / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D002118:Calcium / Q000502:physiology; D016923:Cell Death; D006706:Homeostasis; D006801:Humans; D008274:Magnesium / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D017741:Survivors; D050053:TRPM Cation Channels / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate; D050053:TRPM Cation Channels; D008274:Magnesium; D002118:Calcium