About this Research Topic
Mutations in genes encoding the key components of the cardiac muscle cause diseases referred to as cardiomyopathies. Patients with cardiomyopathies are prone to sudden cardiac death and severe heart failure, which can already manifest at a very young age. The clinical presentation is, however, extremely heterogeneous. Some mutation carriers grow old without ever developing heart disease, whereas others with identical mutations die or develop severe heart failure in their infancy. The presence of a genetic mutation alone is thus not sufficient to explain if and when genetic cardiomyopathy manifests itself, indicating that other factors are at play as well.
In the current issue, we intend to dive deeper into the mechanism by which cardiomyopathy-causing mutations lead to ultrastructural and functional changes in cardiomyocytes. We, therefore, solicit papers that provide insights into the mechanism by which cardiomyopathy-causing mutations lead to ultrastructural and functional changes in cardiomyocytes; focused on gene-environment interactions within the subcellular domain. These may include changes in metabolism and mitochondria, inter-organelle communication, contraction and relaxation defects, and disturbed communication between cardiomyocytes and other cells in the heart.
This Research Topic in Frontiers in Cardiovascular Medicine will publish high-quality research papers, short communications, and reviews covering recent advances in cardiomyopathy research. 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) Ultrastructural organization and disorganization in cells obtained cardiomyopathy hearts of patients and disease models.
2) Second hits (genetic or systemic) that exacerbate cardiomyopathy phenotype.
3) Organellar dysfunction (e.g. mitochondrial) contributing to the cardiomyopathy disease process,
In the current issue, we intend to dive deeper into the mechanism by which cardiomyopathy-causing mutations lead to ultrastructural and functional changes in cardiomyocytes. We, therefore, solicit papers that provide insights into the mechanism by which cardiomyopathy-causing mutations lead to ultrastructural and functional changes in cardiomyocytes; focused on gene-environment interactions within the subcellular domain. These may include changes in metabolism and mitochondria, inter-organelle communication, contraction and relaxation defects, and disturbed communication between cardiomyocytes and other cells in the heart.
This Research Topic in Frontiers in Cardiovascular Medicine will publish high-quality research papers, short communications, and reviews covering recent advances in cardiomyopathy research. 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) Ultrastructural organization and disorganization in cells obtained cardiomyopathy hearts of patients and disease models.
2) Second hits (genetic or systemic) that exacerbate cardiomyopathy phenotype.
3) Organellar dysfunction (e.g. mitochondrial) contributing to the cardiomyopathy disease process,
Keywords: Cardiomyopathy, genetic, metabolism, ultrastructure, second hit, pathophysiology
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.
