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SUMMARY:Mitochondrial Na+ import by the Na+/Ca2+ exchanger NCLX regulates 
 the electron transport chain and ROS production - Dr Antonio Martínez-Rui
 z\, Hospital Univ. Santa Cristina\, Instituto de Investigación Sanitaria 
 Princesa (IIS Princesa)\, Madrid
DTSTART:20220705T140000Z
DTEND:20220705T150000Z
UID:TALK176231@talks.cam.ac.uk
CONTACT:Hannah Burns
DESCRIPTION:Some time ago\, we found that acute hypoxia produces a mitocho
 ndrial superoxide burst that can provide a redox signal driving acute resp
 onses to hypoxia. We searched the mechanism by which mitochondria produces
  superoxide when oxygen concentration decreases\, finding first a role of 
 complex I deactivation in acute hypoxia. Later on\, we have shown that the
  mitochondrial Na+/Ca2+ exchanger NCLX is a key player in this superoxide 
 burst\, so its inhibition abolishes the superoxide burst. Indeed\, we foun
 d two additional surprises. First\, NCLX activation depends on the solubil
 ization of mitochondrial calcium phosphate deposits driven my matrix acidi
 fication after complex I deactivation. Second\, Na+ import influences inne
 r membrane fluidity and coenzyme Q diffusion\, increasing superoxide produ
 ction.\n\nThis mechanism is not operating only in acute hypoxia. We have a
 lso explored the role of mitochondrial Na+ import in hypoxia responses thr
 ough HIF\, inflammation\, and in ischemia-reperfusion injury\, with potent
 ial clinical applications. 
LOCATION:Contact organiser for details
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