Endothelial dysfunction in COVID-19 with smoking

Abstract

Endothelial dysfunction is one of the mechanisms that most likely to play a role in the occurrence of poor clinical outcomes in patients with COVID-19. The hyperinflammatory and pro-coagulation state in COVID-19 suggests an important role for the endothelium, both as an effector contributing to inflammation and thrombosis, as well as a target organ. This state of endothelial dysfunction is also believed to be exacerbated by a history of previous smoking. Tobacco can increase the severity of infectious diseases such as influenza, by increasing viral replication through suppression of antiviral mechanisms, and changes in cytokine patterns in cells also increase ACE2 expression. Smoking is associated with endothelial dysfunction because it can increase the concentration of free radicals and proinflammatory cytokines. So, it is very possible that SARS-CoV-2 will damage the endothelium of smokers who have previously been injured as a result of smoking habits. The literature that we used in this study was obtained through searching engines from the Google Scholar and PubMed databases, with the inclusion criteria being literature that used English. We managed to take 1,613 literature articles, then we selected 81 articles that were most relevant to the discussion of our study. In this study we conclude that endothelial dysfunction may play a role in the mechanism of clinical deterioration in COVID-19 and may be exacerbated by a history of previous smoking.