Investigating the Mechanism of NAD+ Metabolism in Atrial Fibrillation: A Risk Gene Analysis

This study explored potential atrial fibrillation (AF) risk genes via nicotinamide adenine dinucleotide (NAD+) metabolism using tissue samples and the Gene Expression Omnibus (GEO) database.

A cross-sectional study was conducted on atrial tissues from patients undergoing left atrial appendage resection. Whole transcriptome sequencing was performed on 3 AF and 3 control samples. The GSE115574 and GSE79768 datasets were analyzed, yielding 51 NMRGs. DE-mRNAs were screened and overlapped to obtain DE-NMRGs. LASSO and RFE algorithms identified critical genes, and enrichment and drug-prediction analyses were conducted. Gene expressions were validated in 5 additional patients using qRT-PCR.

Three key genes (SLC6A6, ATP1B4, and BEX2) were identified, associated with energy metabolism pathways and potentially influencing AF progression through immune response modulation.

Previous studies reported the role of NAD+ metabolism in AF, but its mechanism is unclear. This study identified SLC6A6, ATP1B4, and BEX2 as gene signatures linking NAD+ metabolism to AF. These genes are involved in metabolic or electrophysiological processes that can predispose to arrhythmogenesis. However, their specific mechanisms of action remain unclear, and further research is needed.

The study identified three key genes (SLC6A6, ATP1B4, and BEX2) involved in NAD+ metabolism, with diagnostic potential for AF patients and associations with energy metabolism and immune infiltration.