Mitochondrial biological function and risk of atrial fibrillation and atrial flutter: A 2-sample Mendelian
Tianyang Zhang1, Hailong Chen1, Yanyu Shi1
1College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Jilin, China.
Abstract:
Current research suggests that mitochondrial dysfunction can be a contributing factor in the development of cardiac arrhythmias. In pursuit of elucidating the causal link between the biological functions of mitochondria and the occurrence of atrial fibrillation/flutter, we conducted a 2-sample Mendelian randomization (MR) study. Mitochondrial proteins were selected for exposure in this study. To enhance the accuracy of our study, we selected data on AF/AFL from the FinnGen study and the UK Biobank for MR analysis, respectively. The inverse variance-weighted method was utilized as the primary analysis technique for MR. In addition, we performed a series of sensitivity analyses to detect heterogeneity and horizontal pleiotropy. MR results indicated a significant positive association between NAD-dependent protein deacylase sirtuin-5 and AF/AFL (odds ratio = 1.084, 95% confidence interval: 1.037-1.133, P = 3.679 × 10-4, Adjusted P = .024), with consistent outcomes observed in replication analysis (odds ratio = 1.002, 95% confidence interval: 1.001-1.003, P = 4.808 × 10-4, Adjusted P = .032). NAD-dependent protein deacylase sirtuin-5 can significantly promote the occurrence of AF/AFL, and its specific mechanisms warrant further investigation.
Insights
Mitochondrial dysfunction is linked to cardiac arrhythmias. This study found NAD-dependent protein deacylase sirtuin-5 significantly promotes atrial fibrillation/flutter (AF/AFL), warranting further mechanistic research.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Genetics
Background:
- Mitochondrial dysfunction is implicated in cardiac arrhythmias.
- Understanding the link between mitochondrial function and atrial fibrillation/flutter (AF/AFL) is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the causal relationship between mitochondrial protein function and the incidence of AF/AFL using a two-sample Mendelian randomization (MR) approach.
Main Methods:
- A two-sample MR study was conducted using genetic data for mitochondrial proteins as exposures.
- Data on AF/AFL were obtained from the FinnGen study and UK Biobank.
- Inverse variance-weighted methods and sensitivity analyses were employed to assess heterogeneity and pleiotropy.
Main Results:
- A significant positive association was found between NAD-dependent protein deacylase sirtuin-5 and AF/AFL (OR=1.084, P=3.679×10⁻⁴).
- Replication analysis confirmed this association (OR=1.002, P=4.808×10⁻⁴).
- NAD-dependent protein deacylase sirtuin-5 was identified as a significant promoter of AF/AFL.
Conclusions:
- NAD-dependent protein deacylase sirtuin-5 plays a significant role in promoting AF/AFL.
- Further research is needed to elucidate the specific molecular mechanisms underlying this association.
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