Mitochondrial DNA heteroplasmy in cardiac tissue from individuals with and without coronary artery disease

Authors

Erik Hefti, Harrisburg University of Science and TechnologyFollow
Javier G. Blanco, The State University of New York at Buffalo

Document Type

Article

Publication Date

5-19-2017

Abstract

The cellular environment associated with coronary artery disease (CAD) can lead to mitochondrial DNA (mtDNA) damage. Mitochondrial variants in some copies of mtDNA (heteroplasmy) and mtDNA content are potential genetic biomarkers for CAD-associated disease states. Massively parallel sequencing and qRT-PCR techniques were used to measure heteroplasmic variants and mtDNA content in heart samples from donors with (n = 8) and without (n = 7) documented CAD. Both groups showed increased numbers of heteroplasmic mtDNA variants in the control region (CR) (p < .0010, ANOVA). The donors with CAD displayed a 41.07% increase in heteroplasmic mtDNA variant number in the CR (p = .043), an 87.50% increase in the number of heteroplasmic mtDNA deletions (p = .12), and a 48.76% increase in the number of heteroplasmic mtDNA single nucleotide variants (p = .029). These data suggest potential trends towards higher cardiac mtDNA heteroplasmy levels in heart samples from donors with CAD.

Recommended Citation

Hefti, E., & Blanco, J. G. (2017). Mitochondrial DNA heteroplasmy in cardiac tissue from individuals with and without coronary artery disease. Mitochondrial DNA Part A, 29 (4), 587-593. ">https://doi.org/10.1080/24701394.2017.1325480

Publication Title

Mitochondrial DNA Part A

Start Page No.

587

End Page No.

593

ISSN

2470-1408

DOI

10.1080/24701394.2017.1325480

Comments

Grant support

R01 GM073646/GM/NIGMS NIH HHS/United States