Journal of Clinical Pathology 2007;60:948-950
SHORT REPORTS
Chronic atrial fibrillation associated with somatic mitochondrial DNA mutations in human atrial tissue
1 Department of Cardiology, Chonnam National University Medical School, Gwangju, South Korea
2 Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, South Korea
3 Departments of Internal Medicine, Wonkwang University Hospital, Iksan, South Korea
4 Department of Thoracic and Cardiovascular Surgery, Wonkwang University Hospital, Iksan, South Korea
5 Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, South Korea
Correspondence to:
Dr Myung-Geun Shin
Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, 160 Ilsimri, Hwasun-eup, Hwasun-gun, Jeollanam-do, South Korea 519-809; mgshin@chonnam.ac.kr
Accepted 17 March 2007
Keywords: chronic atrial fibrillation; atrial tissue; mitochondrial DNA; mutation
| The first 150 words of the full text of this article appear below. |
Somatically acquired mitochondrial DNA (mtDNA) mutations have been linked to aging, degenerative diseases, cancer and organ dysfunction. mtDNA alterations were investigated in matched atrial tissues and blood samples from four patients with chronic atrial fibrillation (cAF) and two matched patients without cAF. Nine novel mtDNA mutations were observed in mtDNA control and coding region. Interestingly, two patients with cAF had tissue-specific length heteroplasmic mutations from nucleotide 16184 to 16193 of the polyC tract and CA repeats starting at nucleotide 514. A 9 bp deletion (nucleotides 8271–8279) in the mtDNA COII gene was only found in tissues and blood cells from two patients with cAF. In patients with cAF, mtDNA mutations, including small deletions and tissue-specific length heteroplasmic mutations, occurred in both mtDNA control and coding regions. These findings strongly suggest that mtDNA mutations may play a crucial role in atrial dysfunction in patients with cAF.
Mitochondria are both the power
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