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Mitochondrial function in thoracic aortic aneurysms

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

Bennett, MR 
Yu, Emma 
Foote, kirsty 

Abstract

Mitochondria contain multiple copies of mitochondrial DNA (mtDNA) that encode ribosomal and transfer RNAs and many essential proteins required for oxidative phosphorylation. Mitochondria are essential for generation of ATP, but also generate reactive oxygen species (ROS) as a by-product of the electron transport chain. Oxidative damage to mitochondrial DNA induces respiratory chain dysfunction, resulting in reduced ATP synthesis and further increased ROS generation. The reduced mitochondrial respiration may be accompanied by increased glycolysis and increased lactate production, and these changes can be detected by reduced oxygen consumption and increased extracellular pH of tissues or cultured cells. Mitochondrial dysfunction leading to reduced mitochondrial respiration has been implicated in both normal vascular ageing and a variety of cardiovascular diseases,, including atherosclerosis, heart failure, and aneurysm formation. For example, reduced mitochondrial DNA (mtDNA) copy number, mitochondrial respiration and expression of specific electron transport chain complexes has been shown in vascular smooth muscle cells (VSMCs) derived from human atherosclerotic plaques1-3. Mitochondriogenesis and mitophagy are also important regulators of mitochondrial health and number. ROS induce VSMC mitophagy, and similarly plaque VSMCs show increased mitophagy compared with normal arterial VSMCs2.

Description

Keywords

Animals, Aorta, Aortic Aneurysm, Thoracic, Extracellular Matrix Proteins, Mice, Mitochondria

Journal Title

Cardiovascular Research

Conference Name

Journal ISSN

0008-6363
1755-3245

Volume Title

Publisher

Oxford University Press
Sponsorship
British Heart Foundation (None)
British Heart Foundation (None)
British Heart Foundation (None)
British Heart Foundation (PG/16/11/32021)
British Heart Foundation (PG/16/63/32307)
British Heart Foundation (CH/2000003)
British Heart Foundation (PG/16/24/32090)
British Heart Foundation (None)
This work was supported by British Heart Foundation (BHF) grants PG/14/69/31032 and RG/13/14/30314, the National Institute for Health Research Cambridge Biomedical Research Centre, the BHF Centre for Research Excellence, the Academy of Medical Sciences.