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Mitochondrial Dysfunction and DNA Damage in the Context of Pathogenesis of Atherosclerosis

1
Institute of Translational Biomedicine, St. Petersburg State University, 199034 St. Petersburg, Russia
2
Department of Basic Research, Institute for Atherosclerosis Research, 121609 Moscow, Russia
3
Federal Scientific Clinical Center for Resuscitation and Rehabilitation, 109240 Moscow, Russia
4
Laboratory of Systemic Rheumatic Disorders, V.A. Nasonova Institute of Rheumatology, 115522 Moscow, Russia
5
Laboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia
6
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
7
Laboratory of Infection Pathology and Molecular Microecology, Institute of Human Morphology, 117418 Moscow, Russia
*
Authors to whom correspondence should be addressed.
Biomedicines 2020, 8(6), 166; https://doi.org/10.3390/biomedicines8060166
Received: 29 May 2020 / Revised: 13 June 2020 / Accepted: 16 June 2020 / Published: 18 June 2020
(This article belongs to the Section Therapeutic Strategies in Different Diseases)
Atherosclerosis is a multifactorial disease of the cardiovascular system associated with aging, inflammation, and oxidative stress. An important role in the development of atherosclerosis play elevated plasma lipoproteins. A number of external factors (smoking, diabetes, infections) can also contribute to the development of the disease. For a long time, atherosclerosis remains asymptomatic, therefore, the search for early markers of the disease is critical for the timely management and better outcomes for patients. Mitochondrial dysfunction and mitochondrial DNA (mtDNA) damage appear to connect different aspects of atherosclerosis pathogenesis. To date, multiple lines of research have demonstrated the strong association of mitochondrial dysfunction with the development of various human diseases. Therapies aimed at restoring the mitochondrial function are being actively developed, and are expected to broaden the therapeutic possibilities for several chronic human diseases. The development of such therapies depends on our understanding of the functional roles of different mtDNA variants associated with one or another disorder, and the molecular mechanisms linking mitochondrial dysfunction with a given pathological feature. These questions are, however, challenging and require future intensive research. This review summarizes the recent studies and describes the central processes of the development of atherosclerosis, and shows their relationship with mitochondrial dysfunction. One of the promising therapeutic approaches for future atherosclerosis treatments is the use of mitochondria-targeted antioxidants. Future studies should focus on characterizing the mechanisms of mitochondrial involvement in cardiovascular pathologies to better direct the search for novel therapies. View Full-Text
Keywords: atherosclerosis; mitochondrial dysfunction; mtDNA damage; oxidative stress; inflammation; antioxidants; endothelial cells atherosclerosis; mitochondrial dysfunction; mtDNA damage; oxidative stress; inflammation; antioxidants; endothelial cells
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MDPI and ACS Style

Shemiakova, T.; Ivanova, E.; Grechko, A.V.; Gerasimova, E.V.; Sobenin, I.A.; Orekhov, A.N. Mitochondrial Dysfunction and DNA Damage in the Context of Pathogenesis of Atherosclerosis. Biomedicines 2020, 8, 166.

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