Key result
FAK inhibition accelerates myofibril maturation and enhances adhesion stability in hiPSC-derived cardiomyocytes.
Focal adhesion kinase (FAK) plays a key role in regulating early steps of de novo myofibrillogenesis and maturation in human cardiomyocytes by modulating focal adhesion dynamics.
Forces generated by myofibrils within cardiomyocytes must be balanced by adhesion to the substrate and to other cardiomyocytes for proper heart function. Loss of this force balance results in cardiomyopathies that ultimately cause heart failure. How this force balance is first established during the assembly of myofibrils is poorly understood. Using human induced pluripotent stem cell derived cardiomyocytes, we show coupling of focal adhesions to myofibrils during early steps of de novo myofibrillogenesis is essential for myofibril maturation. We also establish a key role for Focal adhesion kinase (FAK), a known regulator of adhesion dynamics in non-muscle cells, in regulating focal adhesion dynamics in cardiomyocytes. Specifically, FAK inhibition increased the stability of vinculin in focal adhesions, allowing greater substrate coupling of assembling myofibrils. Furthermore, this coupling is critical for regulating myofibril tension and viscosity. Taken together, our findings uncover a fundamental mechanism regulating the maturation of myofibrils in human cardiomyocytes.
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Taneja et al. (2018) studied Myofibrillogenesis in cardiomyocytes. FAK inhibition (PF-228) or FAK knockdown (siRNA) vs. Control (untreated or scrambled siRNA) was evaluated on Myofibril maturation and adhesion stability. Inhibition of focal adhesion kinase in human induced pluripotent stem cell-derived cardiomyocytes increased adhesion stability and accelerated the maturation of myofibrils.
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