Evidence map›Paper›PMID 41567340›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2025

LncRNA HOTAIR promotes LPS-induced inflammatory responses by activating the NF-κB pathway.

Fengqing Zhu, Zexun Mo, Wuzhou Lin, Cheng Sun, Xiaomei Huang, Meifeng Ye, Hua He, Yujun Li, Kangwei Wang, Juan Zhu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Fengqing Zhu *Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Zexun Mo *Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Wuzhou Lin *Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Cheng SunDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Xiaomei HuangDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Meifeng YeDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Hua HeDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Yujun LiDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Kangwei WangDepartment of Pathology, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, Guangdong, China.
Juan ZhuDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Chuwen LinDepartment of Histology and Embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Shuquan WeiDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Zhike LiangDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Acute Lung InjuryInflammationLipopolysaccharidesNF-kappa BRNA, Long NoncodingSignal TransductionA549 CellsAnimalsCytokinesHumansMaleMiceMice, Inbred C57BLCytokinesHOTAIR long non-coding RNA, mouseHOTAIR long untranslated RNA, humanLipopolysaccharidesNF-kappa BRNA, Long Noncodingacute lung injuryHOTAIRinflammationLncRNANF-κB pathway

Identifiers

PMID41567340
PMCPMC12815884

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.