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Private mitochondrial DNA variants in danish patients with hypertrophic cardiomyopathy.

Authors :
Hagen CM
Aidt FH
Havndrup O
Hedley PL
Jensen MK
Kanters JK
Pham TT
Bundgaard H
Christiansen M
Source :
PloS one [PLoS One] 2015 Apr 29; Vol. 10 (4), pp. e0124540. Date of Electronic Publication: 2015 Apr 29 (Print Publication: 2015).
Publication Year :
2015

Abstract

Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disease primarily caused by mutations in genes coding for sarcomeric proteins. A molecular-genetic etiology can be established in ~60% of cases. Evolutionarily conserved mitochondrial DNA (mtDNA) haplogroups are susceptibility factors for HCM. Several polymorphic mtDNA variants are associated with a variety of late-onset degenerative diseases and affect mitochondrial function. We examined the role of private, non-haplogroup associated, mitochondrial variants in the etiology of HCM. In 87 Danish HCM patients, full mtDNA sequencing revealed 446 variants. After elimination of 312 (69.9%) non-coding and synonymous variants, a further 109 (24.4%) with a global prevalence > 0.1%, three (0.7%) haplogroup associated and 19 (2.0%) variants with a low predicted in silico likelihood of pathogenicity, three variants: MT-TC: m.5772G>A, MT-TF: m.644A>G, and MT-CYB: m.15024G>A, p.C93Y remained. A detailed analysis of these variants indicated that none of them are likely to cause HCM. In conclusion, private mtDNA mutations are frequent, but they are rarely, if ever, associated with HCM.

Details

Language :
English
ISSN :
1932-6203
Volume :
10
Issue :
4
Database :
MEDLINE
Journal :
PloS one
Publication Type :
Academic Journal
Accession number :
25923817
Full Text :
https://doi.org/10.1371/journal.pone.0124540