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Acute cardiac hypoxia produces life-threatening elevations in late sodium current (I LATE ) in the human heart. Here, we show the underlying mechanism: hypoxia induces rapid SUMOylation of Na V 1.5 channels so they reopen when normally inactive, late in the action potential. Na V 1.5 is SUMOylated only on lysine 442, and the mutation of that residue, or application of a deSUMOylating enzyme, prevents hypoxic reopenings. The time course of SUMOylation of single channels in response to hypoxia coincides with the increase in I LATE , a reaction that is complete in under 100 s. In human cardiac myocytes derived from pluripotent stem cells, hypoxia-induced I LATE is confirmed to be SUMO-dependent and to produce action potential prolongation, the pro-arrhythmic change observed in patients.

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