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A central role for ROS in the functional remodelling of L-type Ca2+ channels by hypoxia Peers C; Scragg JL; Boyle JP; Fearon IM; Taylor SC; Green KN; Webster NJ; Ramsden M; Pearson HAPhilos Trans R Soc Lond B Biol Sci 2005[Dec]; 360 (1464): 2247-54Periods of prolonged hypoxia are associated clinically with an increased incidence of dementia, the most common form of which is Alzheimer's disease. Here, we review recent studies aimed at providing a cellular basis for this association. Hypoxia promoted an enhanced secretory response of excitable cells via formation of a novel Ca2+ influx pathway associated with the formation of amyloid peptides of Alzheimer's disease. More strikingly, hypoxia potentiated Ca2+ influx specifically through L-type Ca2+ channels in three distinct cellular systems. This effect was post-transcriptional, and evidence suggests it occurred via increased formation of amyloid peptides which alter Ca2+ channel trafficking via a mechanism involving increased production of reactive oxygen species by mitochondria. This action of hypoxia is likely to contribute to dysregulation of Ca2+ homeostasis, which has been proposed as a mechanism of cell death in Alzheimer's disease. We suggest, therefore, that our data provide a cellular basis to account for the known increased incidence of Alzheimer's disease in patients who have suffered prolonged hypoxic episodes.|Amyloid/*metabolism[MESH]|Apoptosis/physiology[MESH]|Calcium Channels, L-Type/*metabolism[MESH]|Dementia/metabolism/*physiopathology[MESH]|Exocytosis/physiology[MESH]|Homeostasis/*physiology[MESH]|Humans[MESH]|Hypoxia/metabolism/*physiopathology[MESH]|Mitochondria/metabolism[MESH]|Protein Processing, Post-Translational/*physiology[MESH]|Reactive Oxygen Species/*metabolism[MESH] |
