Key result
DM1 sympathetic co-culture increases cardiomyocyte afterdepolarizations to ~55% vs. 15% in controls.
Why the study?
Does sympathetic neuron hyperexcitability contribute to cardiomyocyte electrical instability and arrhythmogenesis (EADs/DADs) in a human iPSC-based myotonic dystrophy type 1 neuro-cardiac co-culture model?
Does sympathetic neuron hyperexcitability contribute to cardiomyocyte electrical instability and arrhythmogenesis (EADs/DADs) in a human iPSC-based myotonic dystrophy type 1 neuro-cardiac co-culture model?
Provides the first experimental evidence in a human iPSC-derived neuro-cardiac microphysiological system that sympathetic neuron hyperexcitability directly exacerbates cardiomyocyte electrical instability and triggers afterdepolarizations in myotonic dystrophy type 1.
Sympathetic hyperexcitability may promote afterdepolarizations in DM1; leaves open whether neuronal targeting alters clinical arrhythmogenesis.
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Reisqs et al. (2026) studied Myotonic dystrophy type 1 (DM1)-associated cardiac arrhythmias (n=20). DM1 (700 CTG repeats) hiPSC-derived sympathetic neuron and cardiomyocyte neuro-cardiac co-culture in a compartmentalized microfluidic device vs. Sex- and age-matched control hiPSC-derived sympathetic neuron and cardiomyocyte co-culture (and monoculture) was evaluated on Incidence of pro-arrhythmogenic early or delayed afterdepolarizations (EADs/DADs) in gap-free recordings of co-cultured hiPSC-CMs (p=<0.0001). Co-culturing DM1 hiPSC-derived cardiomyocytes with DM1 sympathetic neurons increased early or delayed afterdepolarizations to 55% vs 15% in control co-cultures (p<0.0001).
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