Key result
Expression of pseudophosphorylated RLC (S15D) in the hearts of HCM-D166V mice prevented the development of the pathological HCM phenotype and restored systolic and diastolic function.
Constitutive phosphorylation of cardiac myosin regulatory light chain prevents the development of the pathological hypertrophic cardiomyopathy phenotype in a mouse model.
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Supports RLC modification as HCM therapeutic target; leaves open translation from mouse models to patients.
Yuan et al. (2015) studied Hypertrophic cardiomyopathy. Constitutively phosphorylated Serine15 (S15D) mutation vs. Tg-WT and Tg-D166V mice was evaluated on Intact heart function, maximal tension, myofilament Ca(2+) sensitivity, and myofilament structures. Expression of pseudophosphorylated RLC (S15D) in the hearts of HCM-D166V mice prevented the development of the pathological HCM phenotype and restored systolic and diastolic function.
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