REVIEW ARTICLE
Pathophysiology of Acute Respiratory Failure by CoV-2 Infection: Role of Oxidative Stress, Endothelial Dysfunction and Obesity
Rodrigo L. Castillo1, 2, *, Alejandro Gonzaléz-Candia2, 3, Alejandro A. Candia2, 4
Article Information
Identifiers and Pagination:
Year: 2021Volume: 15
Issue: Suppl-1, M4
First Page: 76
Last Page: 81
Publisher ID: TORMJ-15-76
DOI: 10.2174/1874306402115010076
Article History:
Received Date: 28/12/2020Revision Received Date: 15/6/2021
Acceptance Date: 26/6/2021
Electronic publication date: 31/12/2021
Collection year: 2021
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Coronavirus disease 2019 (COVID-19) due to CoV-2 (coronavirus type 2) virus possess a particular risk of developing acute respiratory distress syndrome (ARDS) or SARS (severe acute respiratory syndrome coronavirus 2)-CoV2 in people with pre-existing conditions related to endothelial dysfunction and increased pro-inflammatory and pro-oxidant state. In between these conditions, chronic systemic inflammation related to obese patients is associated with the development of atherosclerosis, type 2 diabetes, and hypertension, comorbidities that adversely affect the clinical outcome in critical patients with COVID-19. Obesity affects up to 40% of the general population in the USA and more than 30% of the adult population in Chile. Until April 2021, 1,019,478 people have been infected, with 23,524 deaths. Given the coexistence of this worldwide obesity epidemic, COVID-19 negative outcomes are seriously enhanced in the current scenario. On the other hand, obesity is characterized by endothelial dysfunction observed in different vascular beds, an alteration which can be associated with impaired vasodilation, oxidative stress, and inflammatory events. Emerging evidence shows that obesity-related conditions such as endothelial dysfunction are associated with detrimental outcomes for COVID-19 evolution, especially if the patient derives to Intensive Care Units (ICU). This implies the need to understand the pathophysiology of the infection in the obese population, in order to propose therapeutic alternatives and public health policies, especially if the virus remains in the population. In this review, we summarize evidence about the pathogeny of Cov-2 infection in obese individuals and discuss how obesity-associated inflammatory and prooxidant status increase the severity of COVID-19.
