Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19-Mechanisms and Therapeutic Targets.
Oxid Med Cell Longev
; 2021: 8671713, 2021.
Article
in English
| MEDLINE | ID: covidwho-1378091
ABSTRACT
The outbreak of the COVID-19 pandemic represents an ongoing healthcare emergency responsible for more than 3.4 million deaths worldwide. COVID-19 is the disease caused by SARS-CoV-2, a virus that targets not only the lungs but also the cardiovascular system. COVID-19 can manifest with a wide range of clinical manifestations, from mild symptoms to severe forms of the disease, characterized by respiratory failure due to severe alveolar damage. Several studies investigated the underlying mechanisms of the severe lung damage associated with SARS-CoV-2 infection and revealed that the respiratory failure associated with COVID-19 is the consequence not only of acute respiratory distress syndrome but also of macro- and microvascular involvement. New observations show that COVID-19 is an endothelial disease, and the consequent endotheliopathy is responsible for inflammation, cytokine storm, oxidative stress, and coagulopathy. In this review, we show the central role of endothelial dysfunction, inflammation, and oxidative stress in the COVID-19 pathogenesis and present the therapeutic targets deriving from this endotheliopathy.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Vascular Diseases
/
Endothelium, Vascular
/
Oxidative Stress
/
Cytokine Release Syndrome
/
SARS-CoV-2
/
COVID-19
/
Inflammation
Type of study:
Observational study
/
Prognostic study
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Oxid Med Cell Longev
Journal subject:
Metabolism
Year:
2021
Document Type:
Article
Affiliation country:
2021
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