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Pandora's Box: mitochondrial defects in ischaemic heart disease and stroke

Published online by Cambridge University Press:  05 April 2017

Sasan Andalib*
Affiliation:
Neuroscience Research Center, Department of Neurosurgery, Poursina Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
Afshin A. Divani
Affiliation:
Department of Neurology, University of Minnesota, Minneapolis, MN, USA Department of Neurosurgery, University of Minnesota, Minneapolis, MN, USA Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN, USA
Tanja M. Michel
Affiliation:
Department of Psychiatry, Psychiatry Region of Southern Denmark, Odense, Denmark Research Unit of Psychiatry, Institute of Clinical Research, University of Southern Denmark, Odense, Denmark Center for Applied Neuroscience, BRIDGE, Odense University Hospital, Psychiatry in the Region of Southern Denmark, University of Southern Denmark, Odense, Denmark
Poul F. Høilund-Carlsen
Affiliation:
Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark Department of Neurology, Neurosciences Research Center, Imamreza Hospital, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Manouchehr S. Vafaee
Affiliation:
Department of Psychiatry, Psychiatry Region of Southern Denmark, Odense, Denmark Research Unit of Psychiatry, Institute of Clinical Research, University of Southern Denmark, Odense, Denmark Center for Applied Neuroscience, BRIDGE, Odense University Hospital, Psychiatry in the Region of Southern Denmark, University of Southern Denmark, Odense, Denmark Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark Department of Neurology, Neurosciences Research Center, Imamreza Hospital, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Albert Gjedde
Affiliation:
Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark Department of Neurology, Neurosciences Research Center, Imamreza Hospital, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada Department of Radiology and Radiological Science, Johns Hopkins University, Baltimore, Maryland, USA
*
*Corresponding author:Sasan Andalib, PhD, Neuroscience Research Center, Department of Neurosurgery, Poursina Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran. Tel: +981333322444; E-mail: [email protected]

Abstract

Ischaemic heart disease and stroke are vascular events with serious health consequences worldwide. Recent genetic and epigenetic techniques have revealed many genetic determinants of these vascular events and simplified the approaches to research focused on ischaemic heart disease and stroke. The pathogenetic mechanisms of ischaemic heart disease and stroke are complex, with mitochondrial involvement (partially or entirely) recently gaining substantial support. Not only can mitochondrial reactive oxygen species give rise to ischaemic heart disease and stroke by production of oxidised low-density lipoprotein and induction of apoptosis, but the impact on pericytes contributes directly to the pathogenesis. Over the past two decades, publications implicate the causative role of nuclear genes in the development of ischaemic heart disease and stroke, in contrast to the potential role of mitochondrial DNA (mtDNA) in the pathophysiology of the disorders, which is much less understood, although recent studies do demonstrate that the involvement of mitochondria and mtDNA in the development of ischaemic heart disease and stroke is likely to be larger than originally thought, with the novel discovery of links among mitochondria, mtDNA and vascular events. Here we explore the molecular events and mtDNA alterations in relation to the role of mitochondria in ischaemic heart disease and stroke.

Type
Review
Copyright
Copyright © Cambridge University Press 2017 

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Footnotes

Co-authors contributed equally.

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