Mitochondrial Na+ import by the Na+/Ca2+ exchanger NCLX regulates the electron transport chain and ROS production

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• Dr Antonio Martínez-Ruiz, Hospital Univ. Santa Cristina, Instituto de Investigación Sanitaria Princesa (IIS Princesa), Madrid
• Tuesday 05 July 2022, 15:00-16:00
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If you have a question about this talk, please contact Hannah Burns.

Some time ago, we found that acute hypoxia produces a mitochondrial superoxide burst that can provide a redox signal driving acute responses 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 found two additional surprises. First, NCLX activation depends on the solubilization of mitochondrial calcium phosphate deposits driven my matrix acidification after complex I deactivation. Second, Na+ import influences inner membrane fluidity and coenzyme Q diffusion, increasing superoxide production.

This mechanism is not operating only in acute hypoxia. We have also explored the role of mitochondrial Na+ import in hypoxia responses through HIF , inflammation, and in ischemia-reperfusion injury, with potential clinical applications.

This talk is part of the MRC Mitochondrial Biology Unit Seminars series.

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