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2000
Volume 26, Issue 8
  • ISSN: 1389-2010
  • E-ISSN: 1873-4316

Abstract

This detailed review disclosed the NF-κB pro-inflammatory gen's activity regulation and explored the therapeutic significance, activation, and inhibition. This study uncovers the structural intricacies of the NF-κB proteins and highlights the key role of SIRT1 in NF-kB signaling pathway regulation. Particularly the Rel Homology Domain (RHD), elucidating interactions and the regulatory mechanisms involving inhibitory proteins like IκB and p100 within the NF-κB signaling cascade. Disruption of the pathway is important in uncontrolled inflammation and immune disorders. This study extensively describes the role connections of canonical and non-canonical signaling pathways of NF-κB with inflammatory and cellular responses. SIRT1 belongs to the class III histone deacetylase, RelA/p65 deacetylation, it regulates the activity of NF-κB, closely linked with the NAD+/NADH cellular ratio, influencing stress responses, aging processes, gene regulation, and metabolic pathways. This detailed study reveals SIRT1 as a crucial avenue for uncovering the role of imbalanced NF-κB in diabetes, obesity, and atherosclerosis. This study provides valuable knowledge about the therapeutic targets of inflammatory disorders.

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2024-04-17
2025-06-17
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  • Article Type:
    Review Article
Keyword(s): Auto-immune; inflammation; metabolic disorder; NF-κB; obesity; signaling pathways; Sirtunin-1
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