Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Jun 25;9(6):137.
doi: 10.3390/biology9060137.

The Role of Mitochondria in Cardiovascular Diseases

Anastasia V Poznyak  1 , Ekaterina A Ivanova  1 , Igor A Sobenin  2   3 , Shaw-Fang Yet  4 , Alexander N Orekhov  5   6
Affiliations
Review

The Role of Mitochondria in Cardiovascular Diseases

Anastasia V Poznyak et al. Biology (Basel). .

Abstract

The role of mitochondria in cardiovascular diseases is receiving ever growing attention. As a central player in the regulation of cellular metabolism and a powerful controller of cellular fate, mitochondria appear to comprise an interesting potential therapeutic target. With the development of DNA sequencing methods, mutations in mitochondrial DNA (mtDNA) became a subject of intensive study, since many directly lead to mitochondrial dysfunction, oxidative stress, deficient energy production and, as a result, cell dysfunction and death. Many mtDNA mutations were found to be associated with chronic human diseases, including cardiovascular disorders. In particular, 17 mtDNA mutations were reported to be associated with ischemic heart disease in humans. In this review, we discuss the involvement of mitochondrial dysfunction in the pathogenesis of atherosclerosis and describe the mtDNA mutations identified so far that are associated with atherosclerosis and its risk factors.

Keywords: atherosclerosis; cardiovascular disease; mitochondria; mitochondrial genome.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

References

    1. Gorman G.S., Chinnery P.F., DiMauro S., Hirano M., Koga Y., McFarland R., Suomalainen A., Thorburn D.R., Zeviani M., Turnbull D.M. Mitochondrial diseases. Nat. Rev. Dis. Primers. 2016;20:16080. doi: 10.1038/nrdp.2016.80. - DOI - PubMed
    1. Kattoor A.J., Pothineni N.V.K., Palagiri D., Mehta J.L. Oxidative Stress in Atherosclerosis. Curr. Atheroscler. Rep. 2017;19:42. doi: 10.1007/s11883-017-0678-6. - DOI - PubMed
    1. Rocha M., Apostolova N., Hernandez-Mijares A., Herance R., Victor V.M. Oxidative stress and endothelial dysfunction in cardiovascular disease: Mitochondria-targeted therapeutics. Curr. Med. Chem. 2010;17:3827–3841. doi: 10.2174/092986710793205444. - DOI - PubMed
    1. Jones D.L., Rodriguez V.J., Alcaide M.L., Barylski N., Cabral D., Rundek T., Weiss S.M., Kumar M. Subclinical atherosclerosis among young and middle-aged adults using carotid intima-media thickness measurements. South Med. J. 2017;110:733–737. doi: 10.14423/SMJ.0000000000000728. - DOI - PMC - PubMed
    1. Boovarahan S.R., Kurian G.A. Mitochondrial dysfunction: A key player in the pathogenesis of cardiovascular diseases linked to air pollution. Rev. Environ. Health. 2018;33:111–122. doi: 10.1515/reveh-2017-0025. - DOI - PubMed