Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 25, Issue 9, Pages 481-487Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2014.06.008
Keywords
mitochondria; atherosclerosis; inflammation
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Funding
- British Heart Foundation [FS/10/70/28507] Funding Source: researchfish
- Medical Research Council [G1000847, G0800784] Funding Source: researchfish
- MRC [G0800784, G1000847] Funding Source: UKRI
- British Heart Foundation [FS/10/70/28507] Funding Source: Medline
- Medical Research Council [G0800784, G1000847] Funding Source: Medline
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Mitochondria are often regarded as the cellular powerhouses through their ability to generate ATP, the universal fuel for metabolic processes. However, in recent years mitochondria have been recognised as critical regulators of cell death, inflammation, metabolism, and the generation of reactive oxygen species (ROS). Thus, mitochondrial dysfunction directly promotes cell death, inflammation, and oxidative stress and alters metabolism. These are key processes in atherosclerosis and there is now evidence that mitochondrial DNA (mtDNA) damage leads to mitochondrial dysfunction and promotes atherosclerosis directly. In this review we discuss the recent evidence for and mechanisms linking mtDNA defects and atherosclerosis and suggest areas of mitochondrial biology that are potential therapeutic targets.
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