About this Research Topic
Endothelial cells (ECs) line the entire circulatory system, forming an interface between circulating blood or lymph in the lumen and rest of the tissue. ECs provide a large surface area of high permeability and play a role in the exchange of gases, fluids, electrolytes, and macromolecules. The interface between blood vessels and tissues act as a barrier, and not only regulate the flow of fluids or substances into and out of a tissue but also control the passage of materials and the transit of white blood cells into and out of the bloodstream. This close relationship between the vascular endothelium and vascularized organs suggests the existence of crosstalk between ECs and these organs, making ECs paramount to vascular biology and manifesting a wide range of homeostatic functions.
Injury of ECs in the vasculature leads to altered barrier functions, which result in various vascular diseases associated with inflammation such as atherosclerosis, hypertension, cardiomyopathy, retinopathy, neuropathy, and cancer. After endothelial injury, vascular repair involves the restoration of the functional endothelial monolayer to recreate a semipermeable barrier. This research topic aims to discuss the recent findings on the mechanisms that regulate endothelial barrier maintenance, endothelial regeneration, endothelial reparative signaling and vascular repair.
Numerous studies have reported the role of endothelial dysregulation in metabolic disorders such as obesity, insulin resistance, dyslipidemia, diabetes mellitus, cognitive defects, and fatty liver disease. However, the role of ECs in regulation of metabolic homeostasis remains poorly understood. This research topic encourages authors to explore ECs communication with metabolic organs such as the liver, islet cells of the pancreas, adipose tissue, cardiac and skeletal muscle, to maintain metabolic homeostasis.
Authors are invited to submit original research articles, reviews, and mini-reviews covering, but not limited to, the following subtopics:
• Recent advances in understanding the role of ECs in homeostasis, thrombosis and fibrinolysis
• Mechanisms regulating EC barrier function
• Endothelial dysfunction (injury) in context with vascular disorders
• Endothelium regeneration and Vascular repair
• Endothelium dysregulation in metabolic disorders
Injury of ECs in the vasculature leads to altered barrier functions, which result in various vascular diseases associated with inflammation such as atherosclerosis, hypertension, cardiomyopathy, retinopathy, neuropathy, and cancer. After endothelial injury, vascular repair involves the restoration of the functional endothelial monolayer to recreate a semipermeable barrier. This research topic aims to discuss the recent findings on the mechanisms that regulate endothelial barrier maintenance, endothelial regeneration, endothelial reparative signaling and vascular repair.
Numerous studies have reported the role of endothelial dysregulation in metabolic disorders such as obesity, insulin resistance, dyslipidemia, diabetes mellitus, cognitive defects, and fatty liver disease. However, the role of ECs in regulation of metabolic homeostasis remains poorly understood. This research topic encourages authors to explore ECs communication with metabolic organs such as the liver, islet cells of the pancreas, adipose tissue, cardiac and skeletal muscle, to maintain metabolic homeostasis.
Authors are invited to submit original research articles, reviews, and mini-reviews covering, but not limited to, the following subtopics:
• Recent advances in understanding the role of ECs in homeostasis, thrombosis and fibrinolysis
• Mechanisms regulating EC barrier function
• Endothelial dysfunction (injury) in context with vascular disorders
• Endothelium regeneration and Vascular repair
• Endothelium dysregulation in metabolic disorders
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.
