COVID-19-associated vasculitis and vasculopathy
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EDITORIAL
COVID‑19‑associated vasculitis and vasculopathy Richard C. Becker1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract The COVID-19 pandemic now totaling 13,000,000 cases and over 571,000 deaths has continued to teach the medical, scientific and lay communities about viral infectious disease in the modern era. Among the many lessons learned for the medical community is the potential for transmissibility and host infectivity of the SARS–CoV-2 virus. Moreover, it has become clear that the virus can affect any organ including the circulatory system, directly via either tissue tropism or indirectly stemming from inflammatory responses in the form of innate immunity, leukocyte debris such as cell-free DNA and histones and RNA viral particles. The following review considers COVID-19-associated vasculitis and vasculopathy as a defining feature of a virus-induced systemic disease with acute, subacute and potential chronic health implications. Keywords COVID-19 · Vasculitis · Vasculopathy
Establishing a foundation for COVID‑19 and vascular pathology The vascular system The vascular system also referred to as the circulatory system or vascular tree carries blood, oxygen and essential elements to all metabolically active tissues and organs of the body and carries waste materials and by-products away. There are five distinct components of the circulatory system: arteries and arterioles (arterial system), veins and venules (venous system) and capillaries (microvascular system) that link arterioles and venules. The dimensions of blood vessels vary by an order of several thousand-fold with capillaries as small as 10 µm to the aorta of 25 mm (Fig. 1). Endothelial cells respond to injury in several stages (reviewed in Abraham). While there may be injurious agent-specific responses, in a majority of cases the initial event is triggered by infection (viral, bacterial), oxidative stress, hypoxia, turbulent blood flow and shear stress, environmental toxins and circulating elements that follow tissue injury with the release of cell-free nucleic acids, histones, chemokines, cytokines and damage-associated proteins. * Richard C. Becker [email protected] 1
University of Cincinnati Heart, Lung and Vascular Institute, 231 Albert Sabin Way, Cincinnati, OH 45267, USA
The two-level response to endothelial cell injury includes an initial rapid response and a slower phenotypic response (reviewed in Abraham) [1]. Briefly, the initial response causes sudden changes in endothelial cell protective or integrity proteins, including nitric oxide, prostaglandins, endothelins, von Willebrand factor (VWF) and tissue plasminogen activator. The slower phenotype response reflects structural changes of endothelial cell topography, cell orientation, basement membranes and surrounding smooth muscle cells. In addition to the extent of initial injury, phenotypic changes follow a response to injury with release of endocrine and paracrine factors, primarily growth factors that provoke the deposition of extracellular
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