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Related Experiment Video

Updated: Jul 14, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
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Cathepsin Levels and Atrial Fibrillation Risk: Insights From Bidirectional and Multivariable Mendelian Randomization

Fang Ye1, Ruya Zhou1, Haiying Lin2

  • 1Department of Cardiology, Lishui People's Hospital, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui, Zhejiang, China.

International Journal of Genomics
|October 31, 2025
PubMed
Summary

Elevated levels of cathepsin O are genetically linked to increased atrial fibrillation (AF) risk. This suggests cathepsins may play a role in AF development, offering potential new therapeutic targets.

Keywords:
atrial fibrillationcardiovascular proteomicscathepsingenetic epidemiologymendelian randomization

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Area of Science:

  • Cardiovascular Genetics
  • Proteomics
  • Molecular Biology

Background:

  • Atrial fibrillation (AF) is a prevalent cardiac arrhythmia with significant health implications.
  • Genome-wide association studies (GWAS) have identified AF risk variants, but the role of proteolytic enzymes like cathepsins is unclear.

Purpose of the Study:

  • To investigate the causal relationship between genetically determined cathepsin levels and atrial fibrillation risk.
  • To explore the role of cathepsins in the pathogenesis of atrial fibrillation using Mendelian randomization.

Main Methods:

  • Utilized bidirectional and multivariable Mendelian randomization (MR) on European ancestry data.
  • Employed genetic instruments for nine cathepsins from the INTERVAL study and AF GWAS meta-analysis data.
  • Performed inverse variance weighted (IVW), MR-Egger, and weighted median analyses, with sensitivity and reverse MR.

Main Results:

  • Genetically elevated cathepsin O levels showed a significant association with increased AF risk (IVW: p=0.0025, OR=1.06).
  • This association for cathepsin O remained robust in multivariable MR analyses.
  • A suggestive association for cathepsin B was observed but did not survive multiple testing correction; reverse causation was not detected.

Conclusions:

  • Provides genetic evidence linking elevated cathepsin O levels to increased AF risk.
  • Suggests cathepsin O, and conditionally cathepsin B, may be causally involved in AF pathogenesis.
  • Highlights proteolytic enzymes as potential therapeutic targets for AF; further validation in diverse cohorts is recommended.