The possible role of nuclear factor erythroid‐2‐related factor 2 activators in the management of Covid‐19

Abstract

COVID‐19 is caused by a novel SARS‐CoV‐2 leading to pulmonary and extra‐pulmonary manifestations due to oxidative stress (OS) development and hyperinflammation. COVID‐19 is primarily asymptomatic though it may cause acute lung injury (ALI), acute respiratory distress syndrome (ARDS), systemic inflammation, and thrombotic events in severe cases. SARS‐CoV‐2‐induced OS triggers the activation of different signaling pathways, which counterbalances this complication. One of these pathways is nuclear factor erythroid 2‐related factor 2 (Nrf2), which induces a series of cellular interactions to mitigate SARS‐CoV‐2‐mediated viral toxicity and OS‐induced cellular injury. Nrf2 pathway inhibits the expression of pro‐inflammatory cytokines and the development of cytokine storm in COVID‐19. Therefore, Nrf2 activators may play an essential role in reducing SARS‐CoV‐2 infection‐induced inflammation by suppressing NLRP3 inflammasome in COVID‐19. Furthermore, Nrf2 activators can attenuate endothelial dysfunction (ED), renin‐angiotensin system (RAS) dysregulation, immune thrombosis, and coagulopathy. Thus this mini‐review tries to clarify the possible role of the Nrf2 activators in the management of COVID‐19. Nrf2 activators could be an effective therapeutic strategy in the management of Covid‐19. Preclinical and clinical studies are recommended in this regard.

The potential role of brain renin‐angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?

“…The conical NF‐κB pathway is triggered in response to the exogenous stimuli through modulation of IκB and the release of NF‐κB which via activation of the negative regulator IκB suppress further release of activated NF‐κB. 118 , 119 Conversely, the non‐conical NF‐κB pathway which involved in the regulation of immune response is activated by endogenous signalling such as TNF‐α via stimulation of NF‐κB inducing kinase. 118 , 120 The normal NF‐κB signalling regulates the survival of the dopaminergic neurons of the SN.…”