The heart is a dynamic environment that is constantly experiencing some degree of remodeling from the point of development, all the way through adulthood. While many genetic components may contribute to the overall presentation of hypertrophic cardiomyopathy (HCM), mutations occurring in sarcomere components such as myosin binding protein C3 (MYBPC3) are of the greatest popularity for study. Aiming to understand the mechanisms underlying heart diseases and to develop effective treatments that circumvent the need for direct patient study, we investigated the use of a platform to mimic the unique physiological conditions of HCM within an in-vitro setting. Following the induction …
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The heart is a dynamic environment that is constantly experiencing some degree of remodeling from the point of development, all the way through adulthood. While many genetic components may contribute to the overall presentation of hypertrophic cardiomyopathy (HCM), mutations occurring in sarcomere components such as myosin binding protein C3 (MYBPC3) are of the greatest popularity for study. Aiming to understand the mechanisms underlying heart diseases and to develop effective treatments that circumvent the need for direct patient study, we investigated the use of a platform to mimic the unique physiological conditions of HCM within an in-vitro setting. Following the induction of mechanical stretch on three human induced pluripotent stem cell derived cardiomyocyte (hiPSC-CM) cell lines containing mutations for MYBPC3 (WT, HET, HOM), all displayed HCM like reactions in calcium waveform. In conclusion, this system demonstrated the potential to apply a constant, static strain to healthy and mutated hiPSC-CMs for the MYBPC3 protein to model HCM in-vitro.
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