ArticleIBRO neuroscience reports2026
LncRNA HOTAIR/miR-9-5p/FOXP1 axis modulates cerebral ischemia-reperfusion injury via NLRP3 inflammasome activation.
Article in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aimed to investigate the association between the HOTAIR-miR-9-5p axis and the inflammatory response in ischemic stroke (IS) and elucidate the underlying molecular mechanisms. Methods: Middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R) were applied to simulate ischemic/reperfusion conditions Results: A significant association was observed between the HOTAIR-miR-9-5p axis and inflammation in both IS patients and MCAO/R mice. HOTAIR was abnormally expressed at a low level, whereas miR-9-5p and the associated protein NLRP3 inflammatory response were increased in the serum of IS patients, as well as in the brain tissue of MCAO/R mice and in SH-SY5Y cells. Mechanistically, miR-9-5p negatively regulated the expression of HOTAIR and FOXP1. Furthermore, HOTAIR was found to regulate NLRP3 expression via the miR-9-5p/FOXP1 pathway. Functional experiments revealed that silencing miR-9-5p protected against cerebral ischemia/reperfusion injury and suppressed NLRP3 inflammasome activation. Conclusion: These findings collectively demonstrate that the HOTAIR/miR-9-5p/FOXP1 axis plays a critical role in NLRP3 inflammasome activation following IS, suggesting that its blockade could be a potential therapeutic strategy for ischemic brain injury.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.