Abstract
Public health globally faces significant risks from conditions like acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and various inflammatory lung disorders. The NF-κB signaling system partially controls lung inflammation, immunological responses, and remodeling. Non-coding RNAs (lncRNAs) are crucial in regulating gene expression. They are increasingly recognized for their involvement in NF-κB signaling and the development of inflammatory lung diseases. Disruption of lncRNA-NF-κB interactions is a potential cause and resolution factor for inflammatory respiratory conditions. This study explores the therapeutic potential of targeting lncRNAs and NF-κB signaling to alleviate inflammation and restore lung function. Understanding the intricate relationship between lncRNAs and NF-κB signaling could offer novel insights into disease mechanisms and identify therapeutic targets. Regulation of lncRNAs and NF-κB signaling holds promise as an effective approach for managing inflammatory lung disorders. This review aims to comprehensively analyze the interaction between lncRNAs and the NF-κB signaling pathway in the context of inflammatory lung diseases. It investigates the functional roles of lncRNAs in modulating NF-κB activity and the resulting inflammatory responses in lung cells, focusing on molecular mechanisms involving upstream regulators, inhibitory proteins, and downstream effectors.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Similar Papers
More From: International Journal of Biological Macromolecules
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.