In cardiac and skeletal muscles, myofilaments are key molecular regulators of the contraction. Indeed, thick-thin filament interactions (via the formation of myosin cross-bridges) lead to force production and motion. In such process, the role of some of the myofilament components remains unclear or ...
In cardiac and skeletal muscles, myofilaments are key molecular regulators of the contraction. Indeed, thick-thin filament interactions (via the formation of myosin cross-bridges) lead to force production and motion. In such process, the role of some of the myofilament components remains unclear or controversial, hence, would require further rigorous investigations. In addition, in many cardiac and skeletal muscle disorders, thick or thin filament proteins have been found to be specifically or preferentially altered. Nevertheless, how these alterations deregulate the contraction is obscure and would need to be addressed. With this understanding, new potential therapeutic interventions are likely to be developed. Thus, in the present research topic contributors are encouraged to submit reviews, mini-reviews, commentaries, perspectives and research articles on these particular aspects.
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