Myosin heavy chain 7 (MYH7)

Myosin heavy chain 7 (MYH7), also known as the cardiac beta-myosin heavy chain (MHC-β), is a major motor protein expressed predominantly in the human cardiac ventricles and slow-twitch (type I) skeletal muscle fibers [1.2.1, 1.2.4]. It functions as an ATPase that converts chemical energy from ATP hydrolysis into mechanical force, facilitating the interaction between thick and thin filaments to drive muscle contraction [1.2.3]. Mutations in the MYH7 gene are a primary cause of inherited heart diseases, including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and left ventricular non-compaction [1.2.5, 1.3.3]. These mutations often lead to hypercontractility or impaired force generation, contributing to pathological remodeling and heart failure [1.2.2]. MYH7 has become a significant therapeutic target with the development of small-molecule modulators such as mavacamten, a first-in-class myosin inhibitor approved for obstructive HCM that reduces excessive actin-myosin cross-bridge formation [1.3.1]. Conversely, myosin activators like omecamtiv mecarbil have been studied for heart failure to enhance systolic function by increasing the number of myosin heads in the force-producing state [1.3.3].

Other names

Cardiac myosin beta heavy chainMHC-betaMYHCBMyosin-7Myosin heavy chain, cardiac muscle, betaCMH1MPD1SPMDSPMMCMD1S

Cardiac myosin inhibitors (e.g., mavacamten, aficamten) bind to the myosin head to reduce the probability of actin-myosin cross-bridge formation, thereby treating hypercontractility in hypertrophic cardiomyopathy. Cardiac myosin activators (e.g., omecamtiv mecarbil, danicamtiv) increase the rate of phosphate release from the myosin-ADP-Pi complex, accelerating the transition to the force-generating state and improving systolic function in heart failure.