Ischemia-induced ionic imbalance leads to the activation of numerous events including mitochondrial dysfunction and eventual cell death. Dysregulation of mitochondrial Ca2+ (Ca2+m) plays a critical role in cell damage under pathological conditions including traumatic brain injury and stroke. High Ca2+m levels can induce the persistent opening of the mitochondrial permeability transition pore and trigger mitochondrial membrane depolarization, Ca2+ release, cessation of oxidative phosphorylation, matrix swelling and eventually outer membrane rupture with release of cytochrome c and other apoptogenic proteins. Thus, the dysregulation of mitochondrial Ca2+ homeostasis is now recognized to play a crucial role in triggering mitochondrial dysfunction and subsequent apoptosis. Recent studies show that some secondary active transport proteins, such as Na+-dependent chloride transporter and Na+/Ca2+ exchanger, contribute to ischemia-induced dissipation of ion homeostasis including Ca2+m
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.