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In cardiovascular disease (CVD), the intricate interplay among endothelial cells, vascular smooth muscle cells (VSMCs), and adventitial fibroblasts is central to the pathological remodeling of blood vessels, a cornerstone of various CVD manifestations. Endothelial cells, constituting the vascular system's inner lining, serve as initial responders to physiological stressors. They regulate vascular tone and integrity by releasing signaling molecules that profoundly influence VSMCs. These cells, responsible for controlling vascular diameter and blood flow, may undergo phenotypic transformations in disease states. Such changes lead to enhanced proliferation, migration, and extracellular matrix protein secretion, contributing to vascular stiffening and atherosclerotic plaque development. Adventitial fibroblasts, located in the vessel's outermost layer, activate and differentiate into myofibroblasts during pathological processes, producing inflammatory mediators and contributing to the fibrotic changes observed in vascular remodeling. The communication between these cell types, facilitated through complex signaling pathways, highlights the complexity of vascular pathology in CVD. A deeper understanding of this cellular dialogue offers critical insights into identifying therapeutic targets to curb vascular remodeling and slow CVD progression.
In this Research Topic, we aim to create a scholarly forum that delves into the latest advances concerning the complex cellular interactions and signaling pathways driving vascular remodeling in cardiovascular disease (CVD). Our focus is on elucidating the roles and underlying mechanisms of endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts in CVD progression. This initiative is designed to enhance our molecular understanding of CVD, paving the way for the identification of innovative therapeutic targets to counteract vascular remodeling and its adverse clinical outcomes.
We welcome original research and review articles in the following topics but not limited to:
- Examination of the interplay between endothelial cells, VSMCs, and adventitial fibroblasts, highlighting relevant signaling pathways and molecular mediators.
- Using machine learning methods, identify relevant characteristic genes in cardiovascular disease.
- Study on the mechanism of anti-myocardial ischemia effect of natural products based on therapeutic angiogenesis
- The role and potential mechanisms of natural products with anti-inflammatory activity in atherosclerosis.
- Critical review of current and future therapeutic interventions aimed at mitigating vascular remodeling.
- Detailed mechanisms of endothelial cell dysfunction and its pivotal role in vascular remodeling within CVD contexts.
- Exploration of endothelial dysfunction as a catalyst for vascular remodeling in CVD, focusing on underlying mechanisms.
- Investigation into the phenotypic shift of vascular smooth muscle cells (VSMCs) towards a synthetic state, its regulatory factors, and consequences for arterial rigidity and plaque development.
- Analysis of the activation and transformation of adventitial fibroblasts into myofibroblasts, including their role in extracellular matrix augmentation and fibrosis during vascular remodeling.
- Assessment of inflammation and immune cell involvement in vascular remodeling processes within CVD.
- Construction of a neural network diagnostic model and investigation of immune infiltration characteristics for Abdominal Aortic Aneurysm
- The potential mechanism and therapy strategies for hypertensive disorders of pregnancy, Kawasaki disease and other relatively rare cardiovascular diseases.
- Study on the pharmacokinetics mechanism of novel natural products with cardiovascular pharmacological activity.
- Analysis of Risk factors and potential mechanism(s) related to cardiovascular diseases, such as adverse intrauterine environment and NAFLD.
In cardiovascular disease (CVD), the intricate interplay among endothelial cells, vascular smooth muscle cells (VSMCs), and adventitial fibroblasts is central to the pathological remodeling of blood vessels, a cornerstone of various CVD manifestations. Endothelial cells, constituting the vascular system's inner lining, serve as initial responders to physiological stressors. They regulate vascular tone and integrity by releasing signaling molecules that profoundly influence VSMCs. These cells, responsible for controlling vascular diameter and blood flow, may undergo phenotypic transformations in disease states. Such changes lead to enhanced proliferation, migration, and extracellular matrix protein secretion, contributing to vascular stiffening and atherosclerotic plaque development. Adventitial fibroblasts, located in the vessel's outermost layer, activate and differentiate into myofibroblasts during pathological processes, producing inflammatory mediators and contributing to the fibrotic changes observed in vascular remodeling. The communication between these cell types, facilitated through complex signaling pathways, highlights the complexity of vascular pathology in CVD. A deeper understanding of this cellular dialogue offers critical insights into identifying therapeutic targets to curb vascular remodeling and slow CVD progression.
In this Research Topic, we aim to create a scholarly forum that delves into the latest advances concerning the complex cellular interactions and signaling pathways driving vascular remodeling in cardiovascular disease (CVD). Our focus is on elucidating the roles and underlying mechanisms of endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts in CVD progression. This initiative is designed to enhance our molecular understanding of CVD, paving the way for the identification of innovative therapeutic targets to counteract vascular remodeling and its adverse clinical outcomes.
We welcome original research and review articles in the following topics but not limited to:
- Examination of the interplay between endothelial cells, VSMCs, and adventitial fibroblasts, highlighting relevant signaling pathways and molecular mediators.
- Using machine learning methods, identify relevant characteristic genes in cardiovascular disease.
- Study on the mechanism of anti-myocardial ischemia effect of natural products based on therapeutic angiogenesis
- The role and potential mechanisms of natural products with anti-inflammatory activity in atherosclerosis.
- Critical review of current and future therapeutic interventions aimed at mitigating vascular remodeling.
- Detailed mechanisms of endothelial cell dysfunction and its pivotal role in vascular remodeling within CVD contexts.
- Exploration of endothelial dysfunction as a catalyst for vascular remodeling in CVD, focusing on underlying mechanisms.
- Investigation into the phenotypic shift of vascular smooth muscle cells (VSMCs) towards a synthetic state, its regulatory factors, and consequences for arterial rigidity and plaque development.
- Analysis of the activation and transformation of adventitial fibroblasts into myofibroblasts, including their role in extracellular matrix augmentation and fibrosis during vascular remodeling.
- Assessment of inflammation and immune cell involvement in vascular remodeling processes within CVD.
- Construction of a neural network diagnostic model and investigation of immune infiltration characteristics for Abdominal Aortic Aneurysm
- The potential mechanism and therapy strategies for hypertensive disorders of pregnancy, Kawasaki disease and other relatively rare cardiovascular diseases.
- Study on the pharmacokinetics mechanism of novel natural products with cardiovascular pharmacological activity.
- Analysis of Risk factors and potential mechanism(s) related to cardiovascular diseases, such as adverse intrauterine environment and NAFLD.
Keywords: vascular remodelling, endothelial cells, vascular smooth muscle cells, adventitial fibroblast
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.
