About this Research Topic
Endothelial cell dysfunction contributes to the pathogenesis of several pathogen-induced hemorrhagic syndromes. The vascular endothelium is a complex system, involved in the regulation of hemostasis, regulation of the defense and the cardiovascular systems. Endothelial cells become activated as part of their homeostatic response (endothelial cell response [ECR]). This can result in a pro- or anti-trombotic, pro- or anti-inflammatory, constricted or hyper-dilatated (permeable) state. If the ECR is not maintained within homeostatic ranges it becomes part of the pathologic mechanism. Numerous infections are characterized by vascular hyper-permeability, microvascular thrombosis and excessive inflammation indicating a prominent role of endothelial cell dysfunction in the pathogenesis of these infectious diseases. The level of dysfunction, determined by the balance between positive and negative feedback mechanisms, contributes to how disease evolves and ultimately the severity of illness. For instance, endothelial cell dysfunction is an important feature of many infection-induced hyper-permeability (e.g., dengue, Hanta, malaria), resulting in plasma leakage and consequently hypovolemia and shock. Integration of a growing molecular understanding of cellular dysfunction with ECR studies will expand our knowledge of disease pathogenesis and find potential targets for intervention. This Research Topic proposes to examine relationships of infection with bacteria, parasites or viruses and endothelial cell dysfunction. The aim of this research topic forum is to highlight the different mechanisms, drivers, modulators of endothelial cell dysfunction, thereby paving the way to identification of potential therapeutic host targets of hemorrhagic fever. We welcome review papers and original articles, but also perspective, hypothesis and opinion papers that highlight recent findings in this area, with particular emphasis on changes that underlie endothelial cell dysfunction. Papers on this topic are expected to stimulate future research to better understand the mechanism of endothelial cell dysfunction in pathogen-induced hemorrhagic fevers.
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