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

dc.check.date2017-06-01
dc.check.infoAccess to this article is restricted until 12 months after publication by the request of the publisher.en
dc.contributor.authorMcCarthy, Cathal M.
dc.contributor.authorKenny, Louise C.
dc.contributor.funderScience Foundation Irelanden
dc.date.accessioned2017-04-10T14:04:06Z
dc.date.available2017-04-10T14:04:06Z
dc.date.issued2016-06-01
dc.date.updated2017-04-10T11:51:57Z
dc.description.abstractMitochondria 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.sponsorshipScience Foundation Ireland (grant number INFANT (12/RC/2272))en
dc.description.statusPeer revieweden
dc.description.versionAccepted Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationMcCarthy, C. M. and Kenny, L. C. (2016) 'Mitochondrial [dys]function; culprit in pre-eclampsia?', Clinical Science, 130(14), pp. 1179-1184. doi:10.1042/cs20160103en
dc.identifier.doi10.1042/cs20160103
dc.identifier.endpage1184en
dc.identifier.issn0143-5221
dc.identifier.issued14en
dc.identifier.journaltitleClinical Scienceen
dc.identifier.startpage1179en
dc.identifier.urihttps://hdl.handle.net/10468/3870
dc.identifier.volume130en
dc.language.isoenen
dc.publisherPortland Press Ltd.en
dc.rights© 2016 The Authors. Published by Portland Press Limited on behalf of the Biochemical Societyen
dc.subjectAntioxidantsen
dc.subjectMitochondriaen
dc.subjectPre-eclampsiaen
dc.subjectReactive oxygen species (ROS)en
dc.titleMitochondrial [dys]function; culprit in pre-eclampsia?en
dc.typeArticle (peer-reviewed)en
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