Role of oxidative dna damage and repair in atrial fibrillation and ischemic heart disease

Liangyu Hu, Zhengkun Wang, Claudia Carmone, Jaap Keijer, Deli Zhang*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

3 Citations (Scopus)

Abstract

Atrial fibrillation (AF) and ischemic heart disease (IHD) represent the two most common clinical cardiac diseases, characterized by angina, arrhythmia, myocardial damage, and cardiac dysfunction, significantly contributing to cardiovascular morbidity and mortality and posing a heavy socio‐economic burden on society worldwide. Current treatments of these two diseases are mainly symptomatic and lack efficacy. There is thus an urgent need to develop novel therapies based on the underlying pathophysiological mechanisms. Emerging evidence indicates that oxidative DNA damage might be a major underlying mechanism that promotes a variety of cardiac diseases, including AF and IHD. Antioxidants, nicotinamide adenine dinucleotide (NAD+) boosters, and enzymes involved in oxidative DNA repair processes have been shown to attenuate oxidative damage to DNA, making them potential therapeutic targets for AF and IHD. In this review, we first summarize the main molecular mechanisms responsible for oxidative DNA damage and repair both in nuclei and mitochondria, then describe the effects of oxidative DNA damage on the development of AF and IHD, and finally discuss potential targets for oxidative DNA repair‐based therapeutic approaches for these two cardiac diseases

Original languageEnglish
Article number3838
JournalInternational Journal of Molecular Sciences
Volume22
Issue number8
DOIs
Publication statusPublished - 7 Apr 2021

Keywords

  • Antioxidant
  • Atrial fibrillation
  • Cardiac disease
  • DNA repair
  • Ischemia/reperfusion injury
  • Ischemic heart disease
  • NAD
  • Oxidative DNA damage
  • PARP1
  • Vitamin B3

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