Mitochondrial Na+ overload is caused by oxidative stress and leads to activation of the caspase 3-dependent apoptotic machinery

Yang K.-T.Pan S.-F.CHUNG-LIANG CHIENHsu S.-M.Tseng Y.-Z.Wang S.-M.Wu M.-L.2020-02-272020-02-2720040892-6638https://www.scopus.com/inward/record.uri?eid=2-s2.0-9444242061&doi=10.1096%2ffj.03-1038fje&partnerID=40&md5=e5cff9f6b075d5f3bff9951d7576920dhttps://scholars.lib.ntu.edu.tw/handle/123456789/465028[SDGs]SDG3caspase 3; hydrogen peroxide; sodium calcium exchange protein; sodium ion; animal cell; apoptosis; article; calcium cell level; cardiovascular disease; controlled study; heart muscle cell; membrane potential; mitochondrial membrane; mitochondrion; nonhuman; oxidative stress; priority journal; signal transduction; sodium cell level; Apoptosis; Calcium; Caspase 3; Caspases; Cytochromes c; Cytosol; Enzyme Activation; Hydrogen Peroxide; Mitochondria; Myocytes, Cardiac; Oxidative Stress; Signal Transduction; Sodium; Sodium-Calcium Exchanger; AnimaliaMitochondrial Na+ overload is caused by oxidative stress and leads to activation of the caspase 3-dependent apoptotic machineryjournal article10.1096/fj.03-1038fje152317302-s2.0-9444242061