人類心房顫動組織中，粒線體基因常見型刪除性突變
Date Issued
2001
Date
2001
Author(s)
賴凌平
DOI
892314B002451
Abstract
Objective: Accumulation of somatic mutations of
mitochondrial DNA (mtDNA) contributes to aging
process and progressive organ dysfunction. We
investigated the common type 4977-base pair mtDNA
deletion (mtDNA 4977 ) in human atrial tissue and
correlated the amount of mtDNA 4977 to clinical atrial fibrillation (AF). Methods: Atrial tissue from the right atrial appendage
was obtained in 88 patients during open heart surgery (48 male and 40 female, 22 children/adolescents and
66 adults). The amount of mtDNA 4977 was measured
using a nested polymerase chain reaction protocol and
normalized to wild type mtDNA.
Results: We found that the mtDNA 4977 was absent in
all 22 pediatric/adolescent patients. In the adult group,
the relative amount of mtDNA 4977 was significantly
higher in patients with AF than in patients without AF
(0.55 ± 0.26 vs 0.35 ± 0.29, p<0.007). The amount of
mtDNA 4977 was also positively associated with age
(r=0.29, p<0.01). Other clinical parameters did not
influence the amount of mtDNA 4977 significantly.
Further multi-variate analysis showed that both aging
and AF contributed independently to the accumulation
of mtDNA 4977 .
Conclusions: AF is associated with an increase of
mtDNA 4977 . This change is similar to the aging process
of atrial tissue and might contribute to atrial
dysfunction in AF.
Subjects
atrial fibrillation
mitochondria
molecular
biology
biology
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
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