Mitochondrial [dys]function; culprit in pre-eclampsia?

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dc.contributor.author McCarthy, Cathal M.
dc.contributor.author Kenny, Louise C.
dc.date.accessioned 2017-04-10T14:04:06Z
dc.date.available 2017-04-10T14:04:06Z
dc.date.issued 2016-06-01
dc.identifier.citation McCarthy, C. M. and Kenny, L. C. (2016) 'Mitochondrial [dys]function; culprit in pre-eclampsia?', Clinical Science, 130(14), pp. 1179-1184. doi:10.1042/cs20160103 en
dc.identifier.volume 130 en
dc.identifier.issued 14 en
dc.identifier.startpage 1179 en
dc.identifier.endpage 1184 en
dc.identifier.issn 0143-5221
dc.identifier.uri http://hdl.handle.net/10468/3870
dc.identifier.doi 10.1042/cs20160103
dc.description.abstract Mitochondria are extensively identified for their bioenergetic capacities; however, recently these metabolic hubs are increasingly being appreciated as critical regulators of numerous cellular signalling systems. Mitochondrial reactive oxygen species have evolved as a mode of cross-talk between mitochondrial function and physiological systems, to sustain equipoise and foster adaption to cellular stress. Redox signalling mediated by exaggerated mitochondrial-ROS (reactive oxygen species) has been incriminated in a plethora of disease pathologies. Excessive production of mitochondrial ROS is intrinsically linked to mitochondrial dysfunction. Furthermore, mitochondrial dysfunction is a key facilitator of oxidative stress, inflammation, apoptosis and metabolism. These are key pathogenic intermediaries of pre-eclampsia, hence we hypothesize that mitochondrial dysfunction is a pathogenic mediator of oxidative stress in the pathophysiology of pre-eclampsia. We hypothesize that mitochondrial-targeted antioxidants may restrain production of ROS-mediated deleterious redox signalling pathways. If our hypothesis proves correct, therapeutic strategies directly targeting mitochondrial superoxide scavenging should be actively pursued as they may alleviate maternal vascular dysfunction and dramatically improve maternal and fetal health worldwide. en
dc.description.sponsorship Science Foundation Ireland (grant number INFANT (12/RC/2272)) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Portland Press Ltd. en
dc.rights © 2016 The Authors. Published by Portland Press Limited on behalf of the Biochemical Society en
dc.subject Antioxidants en
dc.subject Mitochondria en
dc.subject Pre-eclampsia en
dc.subject Reactive oxygen species (ROS) en
dc.title Mitochondrial [dys]function; culprit in pre-eclampsia? en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Cathal McCarthy, Obstetrics & Gynaecology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: cmccarthy@ucc.ie en
dc.internal.availability Full text available en
dc.check.info Access to this article is restricted until 12 months after publication by the request of the publisher. en
dc.check.date 2017-06-01
dc.date.updated 2017-04-10T11:51:57Z
dc.description.version Accepted Version en
dc.internal.rssid 350572797
dc.contributor.funder Science Foundation Ireland en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Clinical Science en
dc.internal.copyrightchecked Yes en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress cmccarthy@ucc.ie en


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