Lectures and seminars MolMet Webinar: Mike Murphy
Welcome to the MolMet webinar with Professor Mike Murphy from the MRC Mitochondrial Biology Unit, University of Cambridge, UK.
Title of his talk: Mitochondria superoxide production in cardiac ischemia-reperfusion injury
Speaker
Mike Murphy, Professor of Mitochondrial Redox Biology
MRC Mitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK
Title
Mitochondria superoxide production in cardiac ischemia-reperfusion injury
Join the webinar
ZOOM ID: 67491653785
Further reading
Mitochondrial redox metabolism is central to the life and death of the cell. Consequently mitochondrial function and dysfunction have turned out to be so central to biomedical questions as diverse as innate immunity, oxygen sensing and response to viral infections. Therefore, we want to know more about how mitochondria function and go wrong in vivo as well as developing therapies focused on preventing mitochondrial damage. In both these areas the development of biological chemistry approaches is a clear way to both develop new probes of mitochondrial function in vivo and in coming up with new therapies. For example, mitochondrial production of free radicals and subsequent oxidative damage has long been known to contribute to damage in conditions such as ischaemia-reperfusion (IR) injury in stroke and heart attack.
Over the past years we have developed a series of mitochondria-targeted compounds designed to ameliorate or determine how these changes occur. I will outline some of this work, which suggested that ROS production in IR injury during stroke 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 succinate 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 to impact on the damage that mitochondrial ROS do in pathology and also to explore how mitochondrial ROS can act as redox signals. I will discuss how these unexpected mechanisms may lead to redox and metabolic signals from mitochondria in a range of conditions under both healthy and pathological conditions.