Cardiovascular disease is a leading cause of death in developed countries and is rapidly spreading in developing countries. Despite the widespread use of currently available treatments, cardiovascular disease persists. Endothelial cells are an essential component to blood and lymphatic vessels and thus their dysfunction plays a critical role in cardiovascular disease (CVD). Endothelial dysfunction encompasses a pro-inflammatory endothelium, reduced vascular growth, and altered vascular remodeling. These pathological conditions result, in part, from altered protein trafficking. Proteins both on the surface of endothelial cells and within are subject to recycling and/or degradation. The dysregulation of this process can result in the alteration of the receptors available on the cell surface. The alteration of these proteins causes changes in both cell function and signaling. Furthermore, dysregulation of protein trafficking including endocytic trafficking can result in the accumulation of aggregated proteins within the cell ultimately resulting in endothelial cell death and promoting a pro-inflammatory environment. Studying the mechanisms that control this process will provide further understanding of the pathophysiology of cardiovascular disease and novel therapeutic strategies. This Research Topic provides a comprehensive overview of protein trafficking in endothelial cells, the role of this process in the dysfunction of these cells and the development and progression of cardiovascular disease, as well as new potential therapeutic strategies.
Together with endothelial cells, vascular smooth muscle cells (VSMCs) are another major component of vascular wall. An important property of VSMCs is phenotypic plasticity where, in response to diverse environmental cues, contractile VSMCs can switch to a “synthetic” phenotype that is characterized by increased motility and proliferation as well as reduced expression of contractile proteins. VSMC plasticity is observed in many vascular diseases in humans including intimal hyperplasia after angioplasty, atherosclerosis, restenosis following vascular interventions or transplant vasculopathy where synthetic VSMC contribute to the progression of intimal lesions that compromise vessel patency. Recent studies have highlighted the important role of VSMCs in the progression of the lesion formation. Restricting VSMCs to the contractile phenotype or blocking the switch to synthetic phenotype has been shown to be an effective strategy to alleviate proliferative vascular disease. Therefore identification of key players and elucidating how they control smooth muscle phenotype is not only critical for a greater understanding of how vascular disease develops and progresses but is necessary to for the development of novel therapeutic targets in the treatment of occlusive vascular wall diseases.
The Topic Editors welcome various types of articles, such as original research, review articles, methodology articles or other article types regarding functional roles of endothelial cells and VSMCs in the lesion formation.
Cardiovascular disease is a leading cause of death in developed countries and is rapidly spreading in developing countries. Despite the widespread use of currently available treatments, cardiovascular disease persists. Endothelial cells are an essential component to blood and lymphatic vessels and thus their dysfunction plays a critical role in cardiovascular disease (CVD). Endothelial dysfunction encompasses a pro-inflammatory endothelium, reduced vascular growth, and altered vascular remodeling. These pathological conditions result, in part, from altered protein trafficking. Proteins both on the surface of endothelial cells and within are subject to recycling and/or degradation. The dysregulation of this process can result in the alteration of the receptors available on the cell surface. The alteration of these proteins causes changes in both cell function and signaling. Furthermore, dysregulation of protein trafficking including endocytic trafficking can result in the accumulation of aggregated proteins within the cell ultimately resulting in endothelial cell death and promoting a pro-inflammatory environment. Studying the mechanisms that control this process will provide further understanding of the pathophysiology of cardiovascular disease and novel therapeutic strategies. This Research Topic provides a comprehensive overview of protein trafficking in endothelial cells, the role of this process in the dysfunction of these cells and the development and progression of cardiovascular disease, as well as new potential therapeutic strategies.
Together with endothelial cells, vascular smooth muscle cells (VSMCs) are another major component of vascular wall. An important property of VSMCs is phenotypic plasticity where, in response to diverse environmental cues, contractile VSMCs can switch to a “synthetic” phenotype that is characterized by increased motility and proliferation as well as reduced expression of contractile proteins. VSMC plasticity is observed in many vascular diseases in humans including intimal hyperplasia after angioplasty, atherosclerosis, restenosis following vascular interventions or transplant vasculopathy where synthetic VSMC contribute to the progression of intimal lesions that compromise vessel patency. Recent studies have highlighted the important role of VSMCs in the progression of the lesion formation. Restricting VSMCs to the contractile phenotype or blocking the switch to synthetic phenotype has been shown to be an effective strategy to alleviate proliferative vascular disease. Therefore identification of key players and elucidating how they control smooth muscle phenotype is not only critical for a greater understanding of how vascular disease develops and progresses but is necessary to for the development of novel therapeutic targets in the treatment of occlusive vascular wall diseases.
The Topic Editors welcome various types of articles, such as original research, review articles, methodology articles or other article types regarding functional roles of endothelial cells and VSMCs in the lesion formation.
