Cardiovascular diseases (CVDs) are one of the leading causes of premature death and chronic disability worldwide, bringing great economic burdens on individuals and society in low and middle-income countries. One type of CVDs mentioned in this Research Topic is about cardiovascular development in congenital heart diseases (CHDs), which is a rare type of CVDs, and the most common birth defects in humans, affecting approximately 1% of the population, and are the leading cause of birth defect-related infant mortality. The genetics and environment could lead to morphologic, physiologic or metabolic abnormities during cardiovascular development that will eventually influence health later in life. It is well known that transcription factors (TFs) are responsible for dictating cardiovascular genes expression and controlling important morphogenetic steps. Most of the inherited forms of CHDs are caused by the mutations in cardiovascular TF genes. Moreover, TFs can powerfully harness the reprogramming of somatic cells into cardiomyocytes, paving the way for potential regenerative therapies. Therefore, a deeper understanding of the transcriptional regulatory mechanisms controlling cardiovascular genes expressions will be critical for deciphering the mechanisms underlying CHDs, as well as for helping to design more powerful and specific regenerative therapies for CVDs.
Additionally, we are also concerned about studying chronic CVDs of adults, including atherosclerosis, thrombosis, myocardial infarction (MI), hypertension, pulmonary arterial hypertension (PAH) and cardiomyopathy, of which the cardiovascular remodeling and regeneration play pivotal roles in the pathogenesis and repair process. Myocardium and vasculature remodeling through the activation of cardiomyocytes, fibroblasts, endothelial cells, smooth muscle cells, interstitial cells and matrix is usually caused by noxious haemodynamic, metabolic or inflammatory stimuli which are induced by physical stress, ischemia or infection. Histopathologically, cardiovascular remodeling involves hyperplasia, interstitial fibrosis, accumulation of extracellular matrices, and/or angiogenesis. The function of TFs in cardiovascular remodeling, especially in the metabolic processes in the cardiovascular field has not been well studied. The metabolism has been identified as determinant responses in regulating cardiac and vascular cell function based on recent findings which have provided critical new pathways in the role of metabolism in CVDs.
The aim of this Research Topic is to gather comprehensive studies on " Transcription factors in cardiovascular development and remodeling ". Original Research and Review articles addressing these and related issues, including those manuscripts presenting new findings or reviewing the field more broadly are welcome for submission. Potential topics include, but are not limited to, the following:
· The TFs underlying the occurrence and progression of CHDs;
·The TFs function in different cells or subcellular structures shared between cardiovascular and other organs and/or diseases;
·The TFs involved in the metabolism in cardiovascular remodeling;
·Recent discoveries about the regulatory network of TFs in animal or in vitro models to reveal pathophysiological and molecular mechanisms of CVDs development or remodeling;
· Screening new biomarkers focused on transcription factors and downstream targets based on sequencing techniques in CVDs diseases.
Cardiovascular diseases (CVDs) are one of the leading causes of premature death and chronic disability worldwide, bringing great economic burdens on individuals and society in low and middle-income countries. One type of CVDs mentioned in this Research Topic is about cardiovascular development in congenital heart diseases (CHDs), which is a rare type of CVDs, and the most common birth defects in humans, affecting approximately 1% of the population, and are the leading cause of birth defect-related infant mortality. The genetics and environment could lead to morphologic, physiologic or metabolic abnormities during cardiovascular development that will eventually influence health later in life. It is well known that transcription factors (TFs) are responsible for dictating cardiovascular genes expression and controlling important morphogenetic steps. Most of the inherited forms of CHDs are caused by the mutations in cardiovascular TF genes. Moreover, TFs can powerfully harness the reprogramming of somatic cells into cardiomyocytes, paving the way for potential regenerative therapies. Therefore, a deeper understanding of the transcriptional regulatory mechanisms controlling cardiovascular genes expressions will be critical for deciphering the mechanisms underlying CHDs, as well as for helping to design more powerful and specific regenerative therapies for CVDs.
Additionally, we are also concerned about studying chronic CVDs of adults, including atherosclerosis, thrombosis, myocardial infarction (MI), hypertension, pulmonary arterial hypertension (PAH) and cardiomyopathy, of which the cardiovascular remodeling and regeneration play pivotal roles in the pathogenesis and repair process. Myocardium and vasculature remodeling through the activation of cardiomyocytes, fibroblasts, endothelial cells, smooth muscle cells, interstitial cells and matrix is usually caused by noxious haemodynamic, metabolic or inflammatory stimuli which are induced by physical stress, ischemia or infection. Histopathologically, cardiovascular remodeling involves hyperplasia, interstitial fibrosis, accumulation of extracellular matrices, and/or angiogenesis. The function of TFs in cardiovascular remodeling, especially in the metabolic processes in the cardiovascular field has not been well studied. The metabolism has been identified as determinant responses in regulating cardiac and vascular cell function based on recent findings which have provided critical new pathways in the role of metabolism in CVDs.
The aim of this Research Topic is to gather comprehensive studies on " Transcription factors in cardiovascular development and remodeling ". Original Research and Review articles addressing these and related issues, including those manuscripts presenting new findings or reviewing the field more broadly are welcome for submission. Potential topics include, but are not limited to, the following:
· The TFs underlying the occurrence and progression of CHDs;
·The TFs function in different cells or subcellular structures shared between cardiovascular and other organs and/or diseases;
·The TFs involved in the metabolism in cardiovascular remodeling;
·Recent discoveries about the regulatory network of TFs in animal or in vitro models to reveal pathophysiological and molecular mechanisms of CVDs development or remodeling;
· Screening new biomarkers focused on transcription factors and downstream targets based on sequencing techniques in CVDs diseases.
