Dr. Hu, Yu-Feng 's publons link picture

Dr. Hu, Yu-Feng

Joint Appointment Associate Research Fellow
  • 02-27899135 (Lab)
  • 02-26523500 (Office)


1. Cardiac arrhythmias

2. Electrophysiology

3. Biological pacemakers

4. Artificial intelligence

Education and Positions:
  • MD. National Cheng-Kung University

    Ph.D. National Yang-Ming University

    Post-doctor fellow, Heart Institute, Cedar Sinai Medical Center, USA

    Attending physician, Division of Cardiology, Taipei Veterans General Hospital.

Highlight Detail

ALDH2 deficiency induces atrial fibrillation through dysregulated cardiac sodium channel and mitochondrial bioenergetics: A multi-omics analysis

Dr. Hu, Yu-Feng
Biochim Biophys Acta Mol Basis Dis. 2021 May 1;1867(5):166088. , May 01, 2021
Point mutation in alcohol dehydrogenase 2 (ALDH2), ALDH2*2 results in decreased catalytic enzyme activity and has been found to be associated with different human pathologies. Whether ALDH2*2 would induce cardiac remodeling and increase the attack of atrial fibrillation (AF) remains poorly understood. The present study evaluated the effect of ALDH2*2 mutation on AF susceptibility and unravelled the underlying mechanisms using a multi-omics approach including whole-genome gene expression and proteomics analysis. The in-vivo electrophysiological study showed an increase in the incidence and reduction in the threshold of AF for the mutant mice heterozygous for ALDH2*2 as compared to the wild type littermates. The microarray analysis revealed a reduction in the retinoic acid signals which was accompanied by a downstream reduction in the expression of voltage-gated Na+ channels (SCN5A). The treatment of an antagonist for retinoic acid receptor resulted in a decrease in SCN5A transcript levels. The integrated analysis of the transcriptome and proteome data showed a dysregulation of fatty acid β-oxidation, adenosine triphosphate synthesis via electron transport chain, and activated oxidative responses in the mitochondria. Oral administration of Coenzyme Q10, an essential co-factor known to meliorate mitochondrial oxidative stress and preserve bioenergetics, conferred a protection against AF attack in the mutant ALDH2*2 mice. The multi-omics approach showed the unique pathophysiology mechanisms of concurrent dysregulated SCN5A channel and mitochondrial bioenergetics in AF. This inspired the development of a personalized therapeutic agent, Coenzyme Q10, to protect against AF attack in humans characterized by ALDH2*2 genotype.