About this Research Topic
After a very successful Volume I, Volume II is now available at https://www.frontiersin.org/research-topics/28153/recent-advances-on-myocardium-physiology-volume-ii
Myocardium is a form of muscle in mammals which has evolved to contract in a repeated fashion, providing blood movement from the heart to the body. Myocardium is composed of cardiac cells; within the cells are myofibrils, as in skeletal muscle cells. Myofibrils contain sarcomeres which are composed of thick (myosin) and thin (actin) filaments, and the giant molecule titin. In myocardial research, since the turn of the 21st century, scientists have applied newly developed molecular biological and optical technologies to ascertain critical details on myocardial contractions under physiological and pathophysiological conditions considering the following topics: ion channel regulation, intracellular Ca2+ dynamics, active or passive properties of sarcomeres in isolated or cultured cardiac cells, and in the beating heart in vivo. Therefore, the application of new technologies to myocardial research will further deepen our understanding of the molecular mechanisms of cardiac function, and provide new prospects to the diagnosis and treatment of various types of heart disease.
This Research Topic in Frontiers in Physiology will publish high quality research papers, short communications, and reviews covering recent advances in myocardial physiology and pathophysiology. We also welcome methods papers describing cutting-edge technologies that can be used to reveal yet unresolved issues in myocardial research. The topics include, but are not limited to, the following categories:
(1) Excitation-contraction coupling
Inside cardiac cells, Ca2+ plays a pivotal role allowing for myofibrils to contract and relax in a repeated fashion. This part of the Research Topic will focus on recent advances on the means by which Ca2+ is mobilized around various organelles of cardiac cells, and how this intracellular Ca2+ mobilization is altered in diseased conditions.
(2) Structure and function of sarcomeres
The binding of Ca2+ to troponin causes structural changes in the thin filament of the cardiac sarcomere, resulting in the onset of actomyosin interaction and the ensuing production of active force. The thick and thin filaments are interconnected by the giant protein titin that acts as a scaffold during myofibrillogenesis and a signaling platform; it forms the basis for passive force. This part of the Research Topic will focus on the emerging roles of thick and thin filament proteins and titin in the modulation of cardiac function in health and disease.
(3) Hypertrophic and dilated cardiomyopathies
Mutations of genes encoding sarcomere proteins (e.g., myosin, troponin, tropomyosin and titin) cause hypertrophic or dilated cardiomyopathies. Hypertrophic cardiomyopathy (HCM) is characterized by enlargement of cardiomyocytes in the left ventricle. Dilated cardiomyopathy (DCM) is characterized by enlargement of cardiac chambers, combined with systolic and diastolic dysfunction. Due to the poor prognosis and malignancy of the heart's pump functions, patients with DCM account for as high as ~ 50% of patients destined for a heart transplant. This part of the Research Topic will focus on recent advances in the molecular mechanisms of the pathogenesis of HCM and DCM, with particular focus on altered relations between excitation-contraction coupling or sarcomere dynamics and the heart’s pump function, and regenerative medicine for diseased hearts.
Myocardium is a form of muscle in mammals which has evolved to contract in a repeated fashion, providing blood movement from the heart to the body. Myocardium is composed of cardiac cells; within the cells are myofibrils, as in skeletal muscle cells. Myofibrils contain sarcomeres which are composed of thick (myosin) and thin (actin) filaments, and the giant molecule titin. In myocardial research, since the turn of the 21st century, scientists have applied newly developed molecular biological and optical technologies to ascertain critical details on myocardial contractions under physiological and pathophysiological conditions considering the following topics: ion channel regulation, intracellular Ca2+ dynamics, active or passive properties of sarcomeres in isolated or cultured cardiac cells, and in the beating heart in vivo. Therefore, the application of new technologies to myocardial research will further deepen our understanding of the molecular mechanisms of cardiac function, and provide new prospects to the diagnosis and treatment of various types of heart disease.
This Research Topic in Frontiers in Physiology will publish high quality research papers, short communications, and reviews covering recent advances in myocardial physiology and pathophysiology. We also welcome methods papers describing cutting-edge technologies that can be used to reveal yet unresolved issues in myocardial research. The topics include, but are not limited to, the following categories:
(1) Excitation-contraction coupling
Inside cardiac cells, Ca2+ plays a pivotal role allowing for myofibrils to contract and relax in a repeated fashion. This part of the Research Topic will focus on recent advances on the means by which Ca2+ is mobilized around various organelles of cardiac cells, and how this intracellular Ca2+ mobilization is altered in diseased conditions.
(2) Structure and function of sarcomeres
The binding of Ca2+ to troponin causes structural changes in the thin filament of the cardiac sarcomere, resulting in the onset of actomyosin interaction and the ensuing production of active force. The thick and thin filaments are interconnected by the giant protein titin that acts as a scaffold during myofibrillogenesis and a signaling platform; it forms the basis for passive force. This part of the Research Topic will focus on the emerging roles of thick and thin filament proteins and titin in the modulation of cardiac function in health and disease.
(3) Hypertrophic and dilated cardiomyopathies
Mutations of genes encoding sarcomere proteins (e.g., myosin, troponin, tropomyosin and titin) cause hypertrophic or dilated cardiomyopathies. Hypertrophic cardiomyopathy (HCM) is characterized by enlargement of cardiomyocytes in the left ventricle. Dilated cardiomyopathy (DCM) is characterized by enlargement of cardiac chambers, combined with systolic and diastolic dysfunction. Due to the poor prognosis and malignancy of the heart's pump functions, patients with DCM account for as high as ~ 50% of patients destined for a heart transplant. This part of the Research Topic will focus on recent advances in the molecular mechanisms of the pathogenesis of HCM and DCM, with particular focus on altered relations between excitation-contraction coupling or sarcomere dynamics and the heart’s pump function, and regenerative medicine for diseased hearts.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
