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Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Naunyn+Schmiedebergs+Arch+Pharmacol 2021 ; 394 (3): 561-567 Nephropedia Template TP
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NF-kappaB signalling as a pharmacological target in COVID-19: potential roles for IKKbeta inhibitors #MMPMID33394134
Kandasamy M
Naunyn Schmiedebergs Arch Pharmacol 2021[Mar]; 394 (3): 561-567 PMID33394134show ga
Coronavirus disease 2019 (COVID-19) has been characterized by lymphopenia as well as a proinflammatory cytokine storm, which are responsible for the poor prognosis and multiorgan defects. The transcription factor nuclear factor-kappaB (NF-kappaB) modulates the functions of the immune cells and alters the gene expression profile of different cytokines in response to various pathogenic stimuli, while many proinflammatory factors have been known to induce NF-kappaB signalling cascade. Besides, NF-kappaB has been known to potentiate the production of reactive oxygen species (ROS) leading to apoptosis in various tissues in many diseases and viral infections. Though the reports on the involvement of the NF-kappaB signalling pathway in COVID-19 are limited, the therapeutic benefits of NF-kappaB inhibitors including dexamethasone, a synthetic form of glucocorticoid, have increasingly been realized. Considering the fact, the abnormal activation of the NF-kappaB resulting from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection might be associated with the pathogenic profile of immune cells, cytokine storm and multiorgan defects. Thus, the pharmacological inactivation of the NF-kappaB signalling pathway can strongly represent a potential therapeutic target to treat the symptomatology of COVID-19. This article signifies pharmacological blockade of the phosphorylation of inhibitor of nuclear factor kappa B kinase subunit beta (IKKbeta), a key downstream effector of NF-kappaB signalling, for a therapeutic consideration to attenuate COVID-19.