In:
Current Neuropharmacology, Bentham Science Publishers Ltd., Vol. 18, No. 11 ( 2020-11-09), p. 1064-1075
Abstract:
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
treatment. 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.
Type of Medium:
Online Resource
ISSN:
1570-159X
DOI:
10.2174/1570159X17666191118125018
Language:
English
Publisher:
Bentham Science Publishers Ltd.
Publication Date:
2020
detail.hit.zdb_id:
2119376-9
