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

doi:10.1016/j.yjmcc.2025.10.008

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Article

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

Journal of molecular and cellular cardiology - 1 Dec 2025

Steczina Sonette, Mohran Saffie, Childers Matthew C, McMillen Timothy S, Naim Ateeqa, Pilagov Matvey, Dente Marica, Kooiker Kristina B, Mandrycky Christian, Tawde Khushi, Hesson Jennifer, Zhao Jing, Mathieu Julie, Pioner J Manuel, Geeves Michael A, Ma Weikang, Moussavi-Harami Farid, Kad Neil M, Regnier Michael

Abstract excerpt

The R403Q mutation in the sarcomere protein beta-myosin heavy chain (β-MHC) is a known genetic cause of hypertrophic cardiomyopathy (HCM), associated with ventricular hypercontractility, impaired relaxation, and cardiac arrhythmias. Despite extensive research, the mutations impact on myosin contractile properties remains unclear partly due to discrepancies across different model systems. In this study, we used a...

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PMID: 41167329
DOI: 10.1016/j.yjmcc.2025.10.008
PMCID: PMC12746836

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