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Review
. 2023 Oct 4;24(19):14876.
doi: 10.3390/ijms241914876.

COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction

Ekaterina Georgieva  1 , Julian Ananiev  1 , Yovcho Yovchev  2 , Georgi Arabadzhiev  2 , Hristo Abrashev  3 , Despina Abrasheva  4 , Vasil Atanasov  5 , Rositsa Kostandieva  5 , Mitko Mitev  6 , Kamelia Petkova-Parlapanska  7 , Yanka Karamalakova  7 , Iliana Koleva-Korkelia  8 , Vanya Tsoneva  9 , Galina Nikolova  7
Affiliations
Review

COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction

Ekaterina Georgieva et al. Int J Mol Sci. .

Abstract

SARS-CoV-2 infection, discovered and isolated in Wuhan City, Hubei Province, China, causes acute atypical respiratory symptoms and has led to profound changes in our lives. COVID-19 is characterized by a wide range of complications, which include pulmonary embolism, thromboembolism and arterial clot formation, arrhythmias, cardiomyopathy, multiorgan failure, and more. The disease has caused a worldwide pandemic, and despite various measures such as social distancing, various preventive strategies, and therapeutic approaches, and the creation of vaccines, the novel coronavirus infection (COVID-19) still hides many mysteries for the scientific community. Oxidative stress has been suggested to play an essential role in the pathogenesis of COVID-19, and determining free radical levels in patients with coronavirus infection may provide an insight into disease severity. The generation of abnormal levels of oxidants under a COVID-19-induced cytokine storm causes the irreversible oxidation of a wide range of macromolecules and subsequent damage to cells, tissues, and organs. Clinical studies have shown that oxidative stress initiates endothelial damage, which increases the risk of complications in COVID-19 and post-COVID-19 or long-COVID-19 cases. This review describes the role of oxidative stress and free radicals in the mediation of COVID-19-induced mitochondrial and endothelial dysfunction.

Keywords: COVID-19; RNS; ROS; endothelial damage; inflammation; mitochondrial dysfunction; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The stages of searching: databases, keywords, applicable criteria, and full-text articles assessed for eligibility and included in the current review.
Figure 2
Figure 2
Multiple organ failure in COVID-19 as a function of hyperinflammation and ROS overproduction.
Figure 3
Figure 3
Role of OS and systemic inflammation in COVID-19-related endothelial injury.
Figure 4
Figure 4
Role of mitochondrial dysfunction, mROS production and inflammation in SARS-CoV-2 induced thrombosis [140] modified by Georgieva E et al. Hyperinflammation increases cytokine production, especially of IL-1, IL-6, and TNF-α, while ROS generated during cytokine storm can damage mitochondria and impair their function through oxidative damage to mtDNA.
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