ArticleJournal of inflammation research2025
MALAT1's m
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- The versatile roles of long non-coding RNAs in kidney disease.Nature reviews. Nephrology · 2026Review
- Pyroptosis: Novel Targets in Molecular Mechanisms and Drug Therapy Research for Myocardial Ischemia Reperfusion Injury.Reviews in cardiovascular medicine · 2026Review
- The crucial role of N6-methyladenosine modification in acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis-induced acute kidney injury (SAKI) significantly contributes to renal dysfunction. Long non-coding RNA MALAT1 has been implicated in regulating inflammation and cell death in various diseases. However, its role in SAKI and the underlying mechanisms remain unclear. Methods: A lipopolysaccharide (LPS)-induced SAKI mouse model and LPS-treated TCMK-1 cells were established. METTL3 and MALAT1 were manipulated via lentiviral-mediated knockdown or overexpression. m6A RNA levels were measured using MeRIP-qPCR, while pyroptosis and inflammation were assessed through ELISA, flow cytometry, Western blotting, immunohistochemistry, and immunofluorescence. RNA immunoprecipitation was conducted to confirm the interaction between METTL3 and MALAT1. Results: LPS treatment significantly increased METTL3 and MALAT1 expression and enhanced m Conclusion: METTL3 promotes pyroptosis in SAKI by enhancing the m6A modification of MALAT1. Targeting the METTL3/MALAT1 axis may provide a potential therapeutic strategy for SAKI by mitigating renal inflammation and cell death.
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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.