Abstract
Since the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak emerged, countless efforts are being made worldwide to understand the molecular mechanisms underlying the coronavirus disease 2019 (COVID-19) in an attempt to identify the specific clinical characteristics of critically ill COVID-19 patients involved in its pathogenesis and provide therapeutic alternatives to minimize COVID-19 severity. Recently, COVID-19 has been closely related to sepsis, which suggests that most deceases in intensive care units (ICU) may be a direct consequence of SARS-CoV-2 infection-induced sepsis. Understanding oxidative stress and the molecular inflammation mechanisms contributing to COVID-19 progression to severe phenotypes such as sepsis is a current clinical need in the effort to improve therapies in SARS-CoV-2 infected patients. This article aims to review the molecular pathogenesis of SARS-CoV-2 and its relationship with oxidative stress and inflammation, which can contribute to sepsis progression. We also provide an overview of potential antioxidant therapies and active clinical trials that might prevent disease progression or reduce its severity.
Highlights
Coronavirus disease 2019 (COVID-19) is spreading rapidly all over the world, affecting millions of people [1]
Severe COVID-19 patients share some common characteristics with sepsis [4], such as inflammation, high levels of systemic pro-inflammatory cytokines, immune dysregulation and microthrombosis [34]. This is probably due to the increase in angiotensin II (Ang II) levels caused by the SARS-CoV-2 and ACE2 interaction itself, and/or the interconnection between the inflammation produced by high levels of IL-6 and other pro-inflammatory cytokines and the oxidative stress identified in COVID-19 patients, contributing to tissue damage
New therapies based on avoiding NETosis, blocking inflammation mediated by NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, or blocking the pathway activated through lymph node-specific intercellular adhesion molecule-3-grabbing integrin (L-SIGN), could be feasible strategies to improve critical characteristics related to COVID-19 [101,115]
Summary
Coronavirus disease 2019 (COVID-19) is spreading rapidly all over the world, affecting millions of people [1] It was declared a pandemic by the World Health Organization (WHO) on 11 March of the present year [2] and fears have increased with a more widespread “second wave”. Intensive care unit (ICUs) capacity and resource limitations have been identified as a major bottleneck for proper assistance of COVID-19 patients [13], increasing the risk of adverse outcomes. In this context, the validation of new therapeutic strategies and treatments are of special relevance to reduce disease progression to severe phenotypes
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