ArticleTranslational stroke research2023
Long Non-coding RNA H19 Promotes NLRP3-Mediated Pyroptosis After Subarachnoid Hemorrhage in Rats.
Article in Translational stroke research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
13 citing papers in PubMed, 32 citations in OpenAlex.
- Liquid-liquid phase separation-driven regulated cell death: from molecular mechanisms to therapeutic strategies.Cell death discovery · 2026Review
- Pyroptosis: inflammatory cell death mechanism and its pathological roles in neurological diseases and injuries.Apoptosis : an international journal on programmed cell death · 2025Review
- Hirudin Alleviates Early Brain Injury After Subarachnoid Hemorrhage in Rats via Regulating NLRP3 Inflammasome-Mediated Pyroptosis.Physiological research · 2025Article
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- The role of ACSL4 in stroke: mechanisms and potential therapeutic target.Molecular and cellular biochemistry · 2025Review
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Research progress of early brain Injury in subarachnoid hemorrhage from 2004 to 2024: a bibliometric analysis.Neurosurgical review · 2025Review
- Sphk1/S1P pathway promotes blood-brain barrier breakdown after intracerebral hemorrhage through inducing Nlrp3-mediated endothelial cell pyroptosis.Cell death & disease · 2024Article
- METTL3-mediated m6A modification enhances lncRNA H19 stability to promote endothelial cell inflammation and pyroptosis to aggravate atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Role of transcription factors, noncoding RNAs, epitranscriptomics, and epigenetics in post-ischemic neuroinflammation.Journal of neurochemistry · 2024Review
- PEDF-34 attenuates neurological deficit and suppresses astrocyte-dependent neuroinflammation by modulating astrocyte polarization via 67LR/JNK/STAT1 signaling pathway after subarachnoid hemorrhage in rats.Journal of neuroinflammation · 2024Article
- Dental pulp mesenchymal stem cell-derived exosomes inhibit neuroinflammation and microglial pyroptosis in subarachnoid hemorrhage via the miRNA-197-3p/FOXO3 axis.Journal of nanobiotechnology · 2024Article
- LncRNA GAS5 restrains ISO-induced cardiac fibrosis by modulating mir-217 regulation of SIRT1.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
NLRP3 inflammasomes have been reported to be an essential mediator in the inflammatory response during early brain injury (EBI) following subarachnoid hemorrhage (SAH). Recent studies have indicated that NLRP3 inflammasome-mediated pyroptosis and long non-coding RNA (lncRNA) H19 can participate in the inflammatory response. However, the roles and functions of lncRNA H19 in NLRP3 inflammasome-mediated pyroptosis during EBI after SAH are unknown and need to be further elucidated. NLRP3 inflammasome proteins were significantly elevated in CSF of human with SAH induced EBI and presented a positive correlation with severity. In ipsilateral hemisphere cortex of rats, these NLRP3 inflammasome proteins were also increased and accompanied with upregulation of H19, and both of NLRP3 and H19 were peaked at 24 h after SAH. However, knockdown of H19 markedly decreased the expression of NLRP3 inflammasome proteins at 24 h after SAH in rats and also ameliorated EBI, showing improved neurobehavioral deficits, cerebral edema, and neuronal injury. Moreover, knocking down of H19 downregulated the expression of Gasdermin D (GSDMD) in microglia in SAH rats. Similarly, knockdown of H19 also alleviated OxyHb-induced pyroptosis and NLRP3-mediated inflammasomes activation in primary microglia. Lastly, H19 competitively sponged with rno-miR-138-5p and then upregulated NLRP3 expression in the post-SAH inflammatory response. lncRNA H19 promotes NLRP3-mediated pyroptosis by functioning as rno-miR-138-5p sponge in rats during EBI after SAH, which might provide a potential therapeutic target for post-SAH inflammation regulation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.