Cardiovascular and metabolic diseases (CMDs) are not only the primary cause of death and disability globally but also represent a huge economic burden for society and individuals. Despite the advanced treatment options for CMDs, mortality and morbidity remain high. Thus, there is an urgent need for preventive and curative treatments for these diseases. To reach this unmet goal, a complete understanding of the cellular and molecular mechanisms underlying the development of cardiovascular and metabolic diseases is needed.
At molecular levels, it is clear that epigenetic and transcriptional dysregulation is associated with the pathogenesis of CMD. Particularly, emerging evidence has revealed that epigenetic mechanisms, including DNA methylation histone modifications, chromatin remodeling, and non-coding RNA mechanisms, play an essential role in regulating gene expression during disease progression. Furthermore, because epigenetic changes are reversible, these make them potential treatment or diagnostic targets for cardiovascular and metabolic diseases. Additionally, the gene expression level is regulated by transcription factors (TFs) at the transcriptional level, and by RNA binding proteins (RBPs) at the post-transcriptional level. It remains not fully understood how TFs and RBPs control gene activity associated with CMD. Therefore, understanding the epigenetic regulation changes and the action of TFs and RBPs in CMDs may help develop advanced diagnostics and interventions for CMDs.
Several mechanisms at cellular levels are linked to CMDs development regression, including but not limited to: mitochondria dysfunction, apoptosis, vascular remodeling, and inflammatory response. Understanding the cellular mechanisms that lead to CMDs is important for identifying the novel treatment or diagnostic targets for CMDs.
In this Research Topic, we aim to promote the recent advances in molecular and cellular mechanisms of CMDs in adults and children. We welcome original research articles, brief research reports, case reports, clinical studies, and reviews. We are particularly interested in studies that focus on understanding the mechanisms associated with comorbidities of heart failure, such as hypertension, diabetes mellitus, renal insufficiency, and neurological as well as musculoskeletal conditions.
Cardiovascular and metabolic diseases (CMDs) are not only the primary cause of death and disability globally but also represent a huge economic burden for society and individuals. Despite the advanced treatment options for CMDs, mortality and morbidity remain high. Thus, there is an urgent need for preventive and curative treatments for these diseases. To reach this unmet goal, a complete understanding of the cellular and molecular mechanisms underlying the development of cardiovascular and metabolic diseases is needed.
At molecular levels, it is clear that epigenetic and transcriptional dysregulation is associated with the pathogenesis of CMD. Particularly, emerging evidence has revealed that epigenetic mechanisms, including DNA methylation histone modifications, chromatin remodeling, and non-coding RNA mechanisms, play an essential role in regulating gene expression during disease progression. Furthermore, because epigenetic changes are reversible, these make them potential treatment or diagnostic targets for cardiovascular and metabolic diseases. Additionally, the gene expression level is regulated by transcription factors (TFs) at the transcriptional level, and by RNA binding proteins (RBPs) at the post-transcriptional level. It remains not fully understood how TFs and RBPs control gene activity associated with CMD. Therefore, understanding the epigenetic regulation changes and the action of TFs and RBPs in CMDs may help develop advanced diagnostics and interventions for CMDs.
Several mechanisms at cellular levels are linked to CMDs development regression, including but not limited to: mitochondria dysfunction, apoptosis, vascular remodeling, and inflammatory response. Understanding the cellular mechanisms that lead to CMDs is important for identifying the novel treatment or diagnostic targets for CMDs.
In this Research Topic, we aim to promote the recent advances in molecular and cellular mechanisms of CMDs in adults and children. We welcome original research articles, brief research reports, case reports, clinical studies, and reviews. We are particularly interested in studies that focus on understanding the mechanisms associated with comorbidities of heart failure, such as hypertension, diabetes mellitus, renal insufficiency, and neurological as well as musculoskeletal conditions.
