September 5, 2025Open Access

Molecular mechanisms of altered contraction with the β-myosin R403Q mutation in porcine ventricular muscle and a human stem cell-derived cardiomyocyte model.

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Research shows altered contractility due to the R403Q mutation in β-myosin, indicating implications for hypertrophic cardiomyopathy.

The R403Q mutation leads to persistent contractile dysfunction in ventricles, suggesting myopathy progression.
X-ray diffraction revealed reduced thick filament order in porcine models, correlating with hypercontractility at submaximal calcium levels.
Super-resolution microscopy indicated that elevated ATPase activity in specific zones is significant for understanding myosin behavior.
The study's findings emphasize the differences in contractile properties observed across porcine and stem cell-derived models.

Steczina et al. (2025) studied this question.

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