Year: 2026
Type: article
Abstract: Acute lung injury (ALI) is a disease with an excessive inflammatory response triggered by activating the NF-κB signaling pathway. Our study aims to investigate the role of the long non-coding RNA HOTAIR in ALI-associated hyperinflammation, providing evidence for HOTAIR as a potential therapeutic target for ALI. Here, we examined the contribution of HOTAIR to LPS-induced lung injury using both A549 cell and murine models. LPS stimulation markedly increased HOTAIR expression in A549 cells, accompanied by reduced cell viability and elevated secretion of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. Overexpression of HOTAIR further amplified NF-κB signaling, as indicated by increased phosphorylation of IκBα and p65 and enhanced nuclear translocation of p65, whereas silencing HOTAIR effectively reversed these effects. In vivo , knockdown of HOTAIR significantly mitigated LPS-induced lung injury, reduced inflammatory cytokine production, and suppressed NF-κB activation in mice. Our findings reveal the contribution of HOTAIR to NF-κB–driven inflammatory injury in ALI, offering insight into its regulatory role and informing future exploration of targeted therapeutic approaches.
Authors: Fengqing Zhu, Zexun Mo, Wuzhou Lin, Cheng Sun, Xiaomei Huang, Meifeng Ye, Hua He, Yujun Li, Kangwei Wang, Juan Zhu, Chuwen Lin, Shuquan Wei, Zhike Liang
Language: English
Topic: NF-κB Signaling Pathways
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,950
OpenAlex ID: W7118511432