Tianjin Medical Journal ›› 2019, Vol. 47 ›› Issue (3): 317-321.doi: 10.11958/20181826

Previous Articles     Next Articles

Progress in endoplasmic reticulum stress and atrial fibrillation

ZHANG Xiao-wei,LI Guang-ping,LIU Tong   

  1. Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Department of Cardiology, the Second Hospital of Tianjin Medical University, Tianjin 300211, China
  • Received:2018-11-22 Revised:2019-01-03 Published:2019-03-15 Online:2019-04-24
  • Contact: Tong LIU E-mail:liutongdoc@126.com

Abstract: Atrial fibrillation (AF) is a common clinical persistent arrhythmia and an independent risk factor for stroke and heart failure. However, the exact pathogenesis of AF is not completely clear. Endoplasmic reticulum is a major organelle that regulates protein synthesis, intracellular Ca2+ concentration, oxidative stress level, and induces apoptotic signaling pathways. A variety of pathogenic factors can lead to endoplasmic reticulum stress (ERS), which mainly restores the homeostasis of endoplasmic reticulum through the unfolded protein response (UPR). Excessive activation of ERS can lead to Ca2+ overload of atrial myocytes, imbalance of oxidative stress and apoptosis, playing an important role in the pathogenesis of AF. The purpose of this review is to summarize the research progress of ERS and AF.

Key words: atrial fibrillation, apoptosis, endoplasmic reticulum stress, unfolded protein response, calcium overload