Pulmonary Endothelial Dysfunction and Thrombotic Complications in COVID-19 Patients.

SARS-CoV-2, a new strain of a Coronaviridae virus which presents 79% genetic similarity to the severe acute respiratory syndrome coronavirus (SARS-CoV) has been recently recognized as the cause of a global pandemic by the World Health Organization (WHO) implying a major threat to the world public health. SARS-CoV-2 infects host human cells by binding through the viral spike proteins to the angiotensin-converting enzyme 2 (ACE-2) receptor, fuses with the cell membrane, enters and starts its replication process in order to multiply its viral load. Coronavirus disease (COVID-19) was initially considered a respiratory infection that could cause pneumonia. However, in severe cases, it extends beyond the respiratory system and becomes a multi-organ disease. This transition from localized respiratory infection to multi-organ disease is due to two main complications of COVID-19. On the one hand, the so-called cytokine storm: an uncontrolled inflammatory reaction of the immune system in which defensive molecules become aggressive for the body itself. On the other hand, the formation of a large number of thrombi that can cause myocardial infarction, stroke and pulmonary embolism (PE). The pulmonary endothelium actively participates in these two processes, becoming the last barrier before the virus spreads throughout the body. In this review, we examine the role of the pulmonary endothelium in response to COVID-19, the existence of potential biomarkers and the development of novel therapies to restore vascular homeostasis and to protect/treat these patients. Additionally, we review the thrombotic complications recently observed in COVID-19 patients and its potential threatening sequelae. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).