PITX2-dependent gene regulation in atrial fibrillation and rhythm control

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Atrial fibrillation (AF) is a common arrhythmia. Better prevention and treatment of AF are needed to reduce AF-associated morbidity and mortality. There are several major mechanisms that cause AF in patients, including a genetic predisposition to develop AF. Genome-wide association studies (GWAS) have identified genetic variants associated with AF populations, with the strongest hits clustering on chromosome 4q25, close to the gene for the homeobox transcription factor PITX2. The effect of these common gene variants on cardiac PITX2 mRNA is currently under study. PITX2 protein regulates right-left differentiation of the embryonic heart, thorax, and aorta. PITX2 is expressed in the adult left atrium, but much less so in other heart chambers. Pitx2 deficiency results in electrical and structural remodeling, and impaired repair of the heart in murine models, all of which may influence AF through divergent mechanisms. PITX2 levels and SNPs on chromosome 4q25 may also be a predictor of the effectiveness of anti-arrhythmic drug therapy
Original languageEnglish
Pages (from-to)4019–4026
JournalThe Journal of Physiology
Issue number12
Early online date25 Apr 2017
Publication statusPublished - 15 Jun 2017


  • antiarrhythmic drugs
  • atrial fibrillation
  • gene regulation
  • mouse model
  • Pitx2
  • transcription factors


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