This review uncovers how iPSC-derived cardiomyocytes and sensory neurons model cardiac pain, suggesting important therapeutic implications.
Cardiac pain is difficult to diagnose and treat in part because existing models fail to capture human neuro-cardiac signaling. This review examines how iPSC-derived cardiomyocytes and sensory neurons in co-culture and organoid systems model ischemic and neuro-immune mechanisms, and how such platforms enable regenerative and neuromodulatory translation. We identify key barriers (maturation, heterogeneity, scalability, safety) and propose priorities to bridge discovery and clinical application.
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Liao et al. (2025) studied this question.
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