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Article ; Online: NF-κB Signaling and Inflammation—Drug Repurposing to Treat Inflammatory Disorders?

Annabell Roberti / Laura Elizabeth Chaffey / David R. Greaves

Biology, Vol 11, Iss 372, p

2022  Volume 372

Abstract: NF-κB is a central mediator of inflammation, response to DNA damage and oxidative stress. As a result of its central role in so many important cellular processes, NF-κB dysregulation has been implicated in the pathology of important human diseases. NF-κB ...

Abstract NF-κB is a central mediator of inflammation, response to DNA damage and oxidative stress. As a result of its central role in so many important cellular processes, NF-κB dysregulation has been implicated in the pathology of important human diseases. NF-κB activation causes inappropriate inflammatory responses in diseases including rheumatoid arthritis (RA) and multiple sclerosis (MS). Thus, modulation of NF-κB signaling is being widely investigated as an approach to treat chronic inflammatory diseases, autoimmunity and cancer. The emergence of COVID-19 in late 2019, the subsequent pandemic and the huge clinical burden of patients with life-threatening SARS-CoV-2 pneumonia led to a massive scramble to repurpose existing medicines to treat lung inflammation in a wide range of healthcare systems. These efforts continue and have proven to be controversial. Drug repurposing strategies are a promising alternative to de novo drug development, as they minimize drug development timelines and reduce the risk of failure due to unexpected side effects. Different experimental approaches have been applied to identify existing medicines which inhibit NF-κB that could be repurposed as anti-inflammatory drugs.
Keywords inflammation ; NF-κB ; drug repurposing ; drug development ; autoimmunity ; COVID-19 ; Biology (General) ; QH301-705.5
Subject code 610
Language English
Publishing date 2022-02-01T00:00:00Z
Publisher MDPI AG
Document type Article ; Online
Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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