IMR Press / FBE / Volume 12 / Issue 1 / DOI: 10.2741/E860

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

The role of mitochondria in cardiovascular diseases related to atherosclerosis
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1 Department of Genetics, Cytology and Bioengineering, Faculty of Biology and Medicine, Voronezh State University, Voronezh, Russia
2 Laboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia
3 Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 109240 Moscow, Russia
4 Institute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan Town, Miaoli County 35053, Taiwan R.O.C.
5 Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Sciences, Moscow 125315, Russia
6 Institute of Human Morphology, 3 Tsyurupa Street, Moscow 117418, Russia
Send correspondence to: Alexander N. Orekhov, Institute of Human Morphology, 3 Tsyurupa Street, Moscow 117418, Russia, E-mail:
Front. Biosci. (Elite Ed) 2020, 12(1), 102–112;
Published: 1 January 2020

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.

Oxidative Stress
Figure 1
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