COVID-19 is, in the end, an endothelial disease
By Peter Libby, T. Lüscher. European Heart Journal, 2020
859 citations recorded by the source corpus.
Abstract The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.
Subfields: Immunology, Infectious Diseases, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/45c67f89f20647d5860725cedb1da2b36d7f7099
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Peiqing Liu
- A. Stewart
- S. Luo
- I. Ilyas
- J. Weng
- Zhuoming Li
- Jihong Han
- P. Little
Citations in the corpus
- Fatigue and cognitive impairment in Post-COVID-19 Syndrome: A systematic review and meta-analysis (2021, neutral): “It is also recognized that systemic sequelae including endothelial dysfunction (Libby and Lüscher, 2020), hyperinflammation, autoimmunity, latent viral reactivation (Oronsky et al., 2021), multi-organ pathology, and autonomic nervous system dysfunction can interact with the foregoing in a…”
- Endothelial Dysfunction in Atherosclerotic Cardiovascular Diseases and Beyond: From Mechanism to Pharmacotherapies (2021, background): “These events may all lead to microvascular and endothelial dysfunction, plaque instability, myocardial injury, and infarction, as well as multiple organ failure, in patients with COVID-19, propelling investigators to deduce that COVID-19 is clinically a disease of the endothelium (Libby and Lüscher,”