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.

Medicine
|July 5, 2024
PubMed

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.