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.
Hypothesis| June 01 2016
Mitochondrial [dys]function; culprit in pre-eclampsia?
Cathal Michael McCarthy;
*Department of Obstetrics and Gynaecology, The Irish Centre for Fetal and Neonatal Translational Research (INFANT), University College Cork, Cork, Ireland
Correspondence: Cathal McCarthy (email firstname.lastname@example.org).
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Cathal Michael McCarthy, Louise Clare Kenny; Mitochondrial [dys]function; culprit in pre-eclampsia?. Clin Sci (Lond) 1 July 2016; 130 (14): 1179–1184. doi: https://doi.org/10.1042/CS20160103
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