Hypertrophic Cardiomyopathy β-Cardiac Myosin Mutation (P710R) Leads to Hypercontractility by Disrupting Super Relaxed State

The authors focused on the P710R mutation that dramatically decreased in vitro motility velocity and actin-activated ATPase, in contrast to other β-cardiac myosin mutations. Human induced pluripotent stem cell–cardiomyocytes with the P710R mutation produced significantly increased force compared with isogenic control cells.