Effect of BIN1 on cardiac dysfunction and malignant arrhythmias

Acta Physiol (Oxf). 2020 Mar;228(3):e13429. doi: 10.1111/apha.13429. Epub 2019 Dec 26.


Heart failure (HF) is the end-stage syndrome for most cardiac diseases, and the 5-year morbidity and mortality of HF remain high. Malignant arrhythmia is the main cause of sudden death in the progression of HF. Recently, bridging integrator 1 (BIN1) was discovered as a regulator of transverse tubule function and calcium signalling in cardiomyocytes. BIN1 downregulation is linked to abnormal cardiac contraction, and it increases the possibility of malignant arrhythmias preceding HF. Because of the detectability of cardiac BIN1 in peripheral blood, BIN1 may serve as a predictor of HF and may be useful in therapy development. However, the mechanism of BIN1 downregulation in HF and how BIN1 regulates normal cardiac function under physiological conditions remain unclear. In this review, recent progress in the biological studies of BIN1-related cardiomyocytes and the effect of cardiac dysfunction and malignant arrhythmia will be discussed.

Keywords: Ca2+ leak; action potential; biomarker; bridging integrator 1; calcium transient; cardiac contraction; ion barrier; ryanodine receptor; transverse tubule.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Arrhythmias, Cardiac / metabolism*
  • Arrhythmias, Cardiac / pathology
  • Heart Failure / metabolism*
  • Heart Failure / pathology
  • Humans
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Nuclear Proteins / metabolism*
  • Tumor Suppressor Proteins / metabolism


  • Adaptor Proteins, Signal Transducing
  • BIN1 protein, human
  • Nuclear Proteins
  • Tumor Suppressor Proteins