What is it about?
We have generated first animal model to express the D94A-mutation in MYL2 that was found to be associated with dilated cardiomyopathy phenotype in humans. Our mice closely follow the clinical phenotype and are an excellent research tool to study DCM. The work suggests that MYL2 may serve as a new therapeutic target for dilated cardiomyopathy.
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Why is it important?
Our data suggest that structural perturbations at the level of sarcomeres result in aberrant cardiomyocyte cytoarchitecture and lead to LV chamber dilation and decreased EF, manifesting in systolic dysfunction of D94A hearts.
Perspectives
The D94A-mediated DCM is a rather complex issue, but clearly involves abnormal interactions between the hypocontractile myosin motors and actin–Tm–Tn filaments. Future studies should involve testing these effects at the single myosin molecule level.
Professor Danuta Szczesna-Cordary
University of Miami
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This page is a summary of: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.
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