Method Profile
Chamber area, beating and injury measurements distinguish selected functional, structural and developmental drug responses.
Investigation of early cardiac morphogenesis, cardiotoxicity and stage-dependent developmental effects.
Human pluripotent-stem-cell-derived chamber-like cardiac organoids with myocardial and early endocardial-like components; predominantly early/atrial-like identity.
Low-attachment culture with brightfield chamber/video analysis, calcium imaging and cellular/molecular injury measurements.
Human cardiac tissues
H9 stem-cell-based organoids; formation was also assessed with H1 and urinary-derived iPSCs.
Analysis tools
Brightfield imaging, chamber-area measurement, motion analysis, CCK-8, LDH and stress/inflammatory expression assays.
Interpret morphology and function separately; developmental experiments preserve the distinction between early exposure and exposure after chamber formation.
Benchmark isoproterenol and anthracycline responses; compare thalidomide/acitretin exposure stages with reference conditions.
Formation assessment: N = 8 independent experiments and more than 600 organoids. Each drug endpoint has its own sampling.
Untreated/vehicle conditions, β-blocker control, aspirin reference and alternative developmental windows.
Isoproterenol increased beating; doxorubicin/daunorubicin reduced chamber area. Thalidomide effects depended on exposure stage, with no significant chamber/beating change in the reported later window.
Human stem-cell-derived cardiac organoids formed stable chamber-like structures and registered changes in beating, chamber area and cell injury. Drug comparisons also showed that developmental exposure timing altered the measured response.
