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10.3390/biology11030372

http://scihub22266oqcxt.onion/10.3390/biology11030372
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suck abstract from ncbi


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pmid35336746      Biology+(Basel) 2022 ; 11 (3): ä
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  • NF-kappaB Signaling and Inflammation-Drug Repurposing to Treat Inflammatory Disorders? #MMPMID35336746
  • Roberti A; Chaffey LE; Greaves DR
  • Biology (Basel) 2022[Feb]; 11 (3): ä PMID35336746show ga
  • NF-kappaB 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-kappaB dysregulation has been implicated in the pathology of important human diseases. NF-kappaB activation causes inappropriate inflammatory responses in diseases including rheumatoid arthritis (RA) and multiple sclerosis (MS). Thus, modulation of NF-kappaB 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-kappaB that could be repurposed as anti-inflammatory drugs.
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