Background: Atherosclerosis is a chronic inflammatory condition that affects different
arteries in the human body and often leads to severe neurological complications, such as stroke and
its sequelae. Affected blood vessels develop atherosclerotic lesions in the form of focal thickening
of the intimal layer, so called atherosclerotic plaques.
Objectives: Despite the high priority of atherosclerosis research for global health and the numerous
preclinical and clinical studies conducted, currently, there is no effective pharmacological treatment
that directly impacts atherosclerotic plaques. Many knowledge gaps exist in our understanding of
the mechanisms of plaque formation. In this review, we discuss the role of mitochondria in different
cell types involved in atherogenesis and provide information about mtDNA mutations associated
with the disease.
Results: Mitochondria of blood and arterial wall cells appear to be one of the important factors in
disease initiation and development. Significant experimental evidence connects oxidative stress
associated with mitochondrial dysfunction and vascular disease. Moreover, mitochondrial DNA
(mtDNA) deletions and mutations are being considered as potential disease markers. Further study
of mtDNA damage and associated dysfunction may open new perspectives for atherosclerosis
Conclusion: Mitochondria can be considered as important disease-modifying factors in several
chronic pathologies. Deletions and mutations of mtDNA may be used as potential disease markers.
Mitochondria-targeting antioxidant therapies appear to be promising for the development of treatment
of atherosclerosis and other diseases associated with oxidative stress and chronic inflammation.