Author Correction: SARS-CoV2-mediated suppression of NRF2-signaling reveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate

Olagnier, David; Farahani, Ensieh; Thyrsted, Jacob; Blay-Cadanet, Julia; Herengt, Angela; Idorn, Manja; Hait, Alon Schneider; Hernáez, Bruno; Knudsen, Alice; Iversen, Marie B.; Schilling, Mirjam; Jørgensen, Sofie E.; Thomsen, Mads Rosendahl; Reinert, Line S.; Lappé, Michael; Hoang, Huy-Dung; Gilchrist, Victoria H.; Hansen, Anne Louise; Ottosen, Rasmus; Nielsen, Camilla G.; Møller, Charlotte; Horst, Demi van der; Peri, Suraj; Balachandran, Siddharth; Huang, Jinrong; Jakobsen, Martin R.; Svenningsen, Esben B.; Poulsen, Thomas B.; Bartsch, Lydia; Thielke, Anne; Luo, Yonglun; Alain, Tommy; Rehwinkel, Jan; Alcamı́, Antonio; Hiscott, John; Mogensen, Trine H.; Paludan, Søren R.; Holm, Christian K.

doi:10.1038/s41467-020-19363-y

Cited by 23 publications

(20 citation statements)

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“…Experimental data show that enhancement of the NRF2-pathway reduces macrophage-mediated alveolar damage and induces the expression of antioxidant genes during influenza [ 26 ]. Moreover, a recent study demonstrated that dimethylfumarate inhibits SARS-CoV-2 replication and the expression of associated inflammatory genes [ 27 ]. Therefore, dimethyl fumarate could have a beneficial anti-inflammatory and cytoprotective action in SARS-CoV-2 infection.…”

Section: Disease-modifyng Therapies and Covid-19mentioning

confidence: 99%

Disease-modifying therapies and SARS-CoV-2 vaccination in multiple sclerosis: an expert consensus

et al. 2021

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Coronavirus disease (COVID-19) appeared in December 2019 in the Chinese city of Wuhan and has quickly become a global pandemic. The disease is caused by the severe acute respiratory syndrome coronavirus type-2 (SARS-CoV-2), an RNA beta coronavirus phylogenetically similar to SARS coronavirus. To date, more than 132 million cases of COVID19 have been recorded in the world, of which over 2.8 million were fatal (https://coronavirus.jhu.edu/map.html). A huge vaccination campaign has started around the world since the end of 2020. The availability of vaccines has raised some concerns among neurologists regarding the safety and efficacy of vaccination in patients with multiple sclerosis (MS) taking immunomodulatory or immunosuppressive therapies.

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Section: Disease-modifyng Therapies and Covid-19mentioning

confidence: 99%

Disease-modifying therapies and SARS-CoV-2 vaccination in multiple sclerosis: an expert consensus

et al. 2021

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“…Komaravelli and Casola [ 170 ] have associated respiratory viral infections with the inhibition of nuclear erythroid factor 2-related factor 2 (Nrf2) and activation of NF-κB, phenomena that incline the balance to inflammation and oxidative damage during these infections [ 170 ]. In a study conducted on lung biopsies from patients with COVID-19, the Nrf2 pathway was found to be suppressed, while pharmacological inductors of Nrf2 have been observed to inhibit SARS-CoV-2 replication and the inflammatory response [ 198 ]. On the other hand, it is known that Nrf2 deficiency increases ACE2 availability, while activation produces the opposite, suggesting that Nrf2 activation in COVID-19 patients could reduce ACE2 availability for entry of SARS-CoV-2 in the cell [ 199 ].…”

Section: Role Of Oxidative Stress and Antioxidant System In Patients With Covid-19mentioning

confidence: 99%

“…IRF3 inhibition has been associated with Nrf2 expression since its silencing is enough to restore IRF3 dimerization and limit the effect of 4-OI. The authors propose the use of DMF and 4-OI as Nrf2 agonists that can be used to inhibit SARS-CoV-2 replication as well as the expression of associated inflammatory genes in patients with COVID-19 [ 198 ].…”

Section: Antioxidants As Neuroprotectors In Patients Infected With Covid-19mentioning

confidence: 99%

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

et al. 2021

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Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.

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“…In previous studies, Nrf2 was under-expressed in human coronavirus HCoV-229E which is associated with the common cold and pulmonary edema [ 87 ]. Interestingly, Nrf2 suppression was also found in the lung biopsies of patients with COVID-19 [ 88 ]. In fact, ACE2 expression is also regulated by Nrf2 pathway, and few studies demonstrated that Nrf2 under-expression increases the availability of ACE2 and that may increase the risk of viral infection [ 89 ].…”

Section: Role Of Covid-19 In Redox Imbalance and Mitochondrial Dysfunctionmentioning

confidence: 99%

Neurological Implications of COVID-19: Role of Redox Imbalance and Mitochondrial Dysfunction

2021

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Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 or COVID-19 has been declared as a pandemic disease by the World Health Organization (WHO). Globally, this disease affected 159 million of the population and reported ~ 3.3 million deaths to the current date (May 2021). There is no definitive treatment strategy that has been identified, although this disease has prevailed in its current form for the past 18 months. The main challenges in the (SARS-CoV)-2 infections are in identifying the heterogeneity in viral strains and the plausible mechanisms of viral infection to human tissues. In parallel to the investigations into the patho-mechanism of SARS-CoV-2 infection, understanding the fundamental processes underlying the clinical manifestations of COVID-19 is very crucial for designing effective therapies. Since neurological symptoms are very apparent in COVID-19 infected patients, here, we tried to emphasize the involvement of redox imbalance and subsequent mitochondrial dysfunction in the progression of the COVID-19 infection. It has been articulated that mitochondrial dysfunction is very apparent and also interlinked to neurological symptoms in COVID-19 infection. Overall, this article provides an in-depth overview of redox imbalance and mitochondrial dysfunction involvement in aggravating COVID-19 infection and its probable contribution to the neurological manifestation of the disease.

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Author Correction: SARS-CoV2-mediated suppression of NRF2-signaling reveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 23 publications

References 0 publications

Disease-modifying therapies and SARS-CoV-2 vaccination in multiple sclerosis: an expert consensus

Disease-modifying therapies and SARS-CoV-2 vaccination in multiple sclerosis: an expert consensus

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

Neurological Implications of COVID-19: Role of Redox Imbalance and Mitochondrial Dysfunction

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