[Frontiers in Bioscience, Elite, 12, 102-112, Jan 1, 2020]

The role of mitochondria in cardiovascular diseases related to atherosclerosis

Victor Yu Glanz1, Igor A. Sobenin2, Andrey V. Grechko3, Shaw-Fang Yet4, Alexander N. Orekhov5,6

1Department of Genetics, Cytology and Bioengineering, Faculty of Biology and Medicine, Voronezh State University, Voronezh, Russia, 2Laboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia, 3Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 109240 Moscow, Russia, 4Institute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan Town, Miaoli County 35053, Taiwan R.O.C., 5Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Sciences, Moscow 125315, Russia, 6Institute of Human Morphology, 3 Tsyurupa Street, Moscow 117418, Russia


1. Abstract
2. Introduction
3. Pathogenesis of atherosclerosis
4. Mitochondrial organization and homeostasis
5. Contribution of ROS to atherosclerosis
6. mtDNA and atherosclerosis
7. Future directions
8. Conclusions
9. Acknowledgments
10. References


Atherosclerosis is a complex disorder that involves several mechanisms of pathogenesis tightly related to each other: lipid accumulation, inflammation and structural changes in the arterial wall. The main source of lipids accumulating in the arterial wall is low-density lipoprotein (LDL) atherogenically modified by desialylation or oxidation. Oxidized LDL can be produced as a result of enhanced generation of reactive oxygen species by mitochondria during oxidative stress. Mitochondrial dysfunction was found to be involved in every aspect of atherosclerosis, and is currently evaluated as a potential point of therapeutic intervention. In particular, atherosclerosis-associated inflammation and its link to mitochondrial dysfunction appear to be interesting, since mitochondria not only trigger the response to external signals, but also can act as pro-inflammatory agents themselves. In this regard, atherosclerosis is potentially an autoimmune disease. In this review, we summarize recent insights on the role of mitochondrial dysfunction in atherogenesis and discuss the significance of mitochondria for understanding of molecular basis of cardiovascular diseases.


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Key Words: Atherosclerosis; Inflammation, Mitochondrion, mtDNA, Oxidative Stress

Send correspondence to: Alexander N. Orekhov, Institute of Human Morphology, 3 Tsyurupa Street, Moscow 117418, Russia, Tel: 79031690866, Fax: 79031690866, E-mail: a.h.opexob@gmail.com