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Mitochondrial superoxide production in ischaemia-reperfusion injury| old_uid | 11668 |
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| title | Mitochondrial superoxide production in ischaemia-reperfusion injury |
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| start_date | 2016/05/27 |
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| schedule | 11h30 |
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| online | no |
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| details | Invitant : Giovanni Marsicano, Giovanni Marsicano´s Lab / Neurocentre Magendie |
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| summary | Mitochondrial ROS have long been known to contribute to ischaemia-reperfusion (IR) injury in heart attack and stroke, but methods to stop this ROS production were limited. Over the past few years we have developed a mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing ROS formation in IR injury with therapeutic implications. In addition, the protection by this compound suggested that ROS production in IR injury was mainly coming from complex I.
This led us to investigate the mechanism of the ROS production and using a metabolomic approach we found that the ROS production in IR injury came from the accumulation of citric acid cycle substrates during ischaemia that then drove mitochondrial ROS production by reverse electron transport at complex I during reperfusion.
This surprising mechanism led up to develop further new therapeutic approaches. |
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| responsibles | Deris |
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