Hypoxia Produces Pro-arrhythmic Late Sodium Current in Cardiac Myocytes by SUMOylation of NaV1.5 Channels (Cell Reports)

The cardiac channel NaV1.5 passes pro-arrhythmic late sodium currents in response to hypoxia. Plant et al. demonstrate the pathophysiological mechanism to be rapid, hypoxia-induced monoSUMOylation of NaV1.5 channels. Blocking SUMOylation of lysine442 prevents hypoxia-induced late currents and attendant prolongation of the action potential in human cardiomyocytes derived from pluripotent stem cells.