Heart failure (HF) is a common life-threatening disorder that constitutes a major medical and economic burden worldwide. HF is largely a disease of older people; with the aging of the population, the burden of HF is increasing. It is estimated that by 2030, approximately 8 million adults in the United States will have HF. The financial costs of treating HF are increasing as well, from $30.7 billion spent in 2012 to $69.8 billion projected for 2030. Thus, it is imperative to increase understanding of the molecular mechanisms underlying this disease in order to facilitate the development and implementation of improved therapies and interventions.
The focus of this research topic is the inherited cardiomyopathies, a clinically heterogeneous group of heart muscle disorders. They are divided into dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (AC), and restrictive cardiomyopathy (RCM), based on phenotype defined by clinical evaluation of affected individuals, each of which may be the cause of a HF syndrome. This traditional classification based on structural and functional changes at the whole-organ level, which resulted extensive overlap between these phenotypes in practice.
In recent years, several genome-wide association studies (GWAS) of genetic cardiomyopathies have identified genetic variants associated with HF. More importantly, a recent study found shared genetic pathways contribute to the risk of HCM and DCM , but with opposite directions of effect. Although GWAS studies have been successful on identifying DNA variation implicated in genetic cardiomyopathies, they provide little or no molecular evidence of gene causality. Recent studies have implemented the integration of multi-omics data including transcriptome, epigenome, proteome, metabolome to accelerate the identification of novel mechanisms for cardiovascular disease and understand the dynamics of disease manifestation. The goals of this research topic are using multi-omics approach 1) to better classify the phenotypes of cardiomyopathies; 2) to identify high risk individuals; 3) to understand mechanism of inherited cardiomyopathies and identify potential drug targets.
We welcome all types of manuscripts, including: original basic science reports, review articles, methodology papers, translational research, and clinical studies including, but not limited to:
1) Next generation sequencing, linkage analysis and GWAS of cardiomyopathy phenotypes.
2) The mechanism of newly reported genetic variants in cardiomyopathy phenotypes.
3) Biomarkers of early detection of cardiomyopathies
4) The interactions between genetics and genomic and environmental factors in cardiomyopathy phenotypes and heart failure.
5) New insights of classification and risk stratification of cardiomyopathy phenotypes.
Heart failure (HF) is a common life-threatening disorder that constitutes a major medical and economic burden worldwide. HF is largely a disease of older people; with the aging of the population, the burden of HF is increasing. It is estimated that by 2030, approximately 8 million adults in the United States will have HF. The financial costs of treating HF are increasing as well, from $30.7 billion spent in 2012 to $69.8 billion projected for 2030. Thus, it is imperative to increase understanding of the molecular mechanisms underlying this disease in order to facilitate the development and implementation of improved therapies and interventions.
The focus of this research topic is the inherited cardiomyopathies, a clinically heterogeneous group of heart muscle disorders. They are divided into dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (AC), and restrictive cardiomyopathy (RCM), based on phenotype defined by clinical evaluation of affected individuals, each of which may be the cause of a HF syndrome. This traditional classification based on structural and functional changes at the whole-organ level, which resulted extensive overlap between these phenotypes in practice.
In recent years, several genome-wide association studies (GWAS) of genetic cardiomyopathies have identified genetic variants associated with HF. More importantly, a recent study found shared genetic pathways contribute to the risk of HCM and DCM , but with opposite directions of effect. Although GWAS studies have been successful on identifying DNA variation implicated in genetic cardiomyopathies, they provide little or no molecular evidence of gene causality. Recent studies have implemented the integration of multi-omics data including transcriptome, epigenome, proteome, metabolome to accelerate the identification of novel mechanisms for cardiovascular disease and understand the dynamics of disease manifestation. The goals of this research topic are using multi-omics approach 1) to better classify the phenotypes of cardiomyopathies; 2) to identify high risk individuals; 3) to understand mechanism of inherited cardiomyopathies and identify potential drug targets.
We welcome all types of manuscripts, including: original basic science reports, review articles, methodology papers, translational research, and clinical studies including, but not limited to:
1) Next generation sequencing, linkage analysis and GWAS of cardiomyopathy phenotypes.
2) The mechanism of newly reported genetic variants in cardiomyopathy phenotypes.
3) Biomarkers of early detection of cardiomyopathies
4) The interactions between genetics and genomic and environmental factors in cardiomyopathy phenotypes and heart failure.
5) New insights of classification and risk stratification of cardiomyopathy phenotypes.
