ArticleInternational journal of general medicine2026
METTL16 Promotes Cerebral Ischemia-Reperfusion Injury via m
Article in International journal of general medicine, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ischemic stroke leads to severe cerebral ischemia/reperfusion (I/R) injury, resulting in neuronal death and neurological deficits. The N Methods: A transient middle cerebral artery occlusion (MCAO) model was established in adult male C57BL/6J mice. METTL16 was knocked down via intracerebroventricular injection of shRNA-expressing lentivirus at 6 hours post-reperfusion. Cerebral infarct volume (TTC staining), neurological function (mNSS, adhesive removal, corner-turning, and rotarod tests), histopathology (H&E, TUNEL, Nissl, NeuN), and apoptosis-related protein expression were evaluated. Primary cortical neurons and astrocytes were subjected to oxygen-glucose deprivation (OGD). Cell apoptosis, LDH release, inflammatory cytokines (TNF-α, IL-1β), and synaptic protein (Synapsin-1, PSD-95) expression were assessed. The METTL16-TIPARP interaction and m Results: METTL16 knockdown significantly reduced infarct volume, attenuated neuronal apoptosis and inflammation, and improved sensorimotor and coordination functions after MCAO. In vitro, METTL16 depletion protected neurons and astrocytes from OGD-induced apoptosis, cytokine release, and synaptic damage. Mechanistically, METTL16 directly bound to TIPARP mRNA and enhanced its m Conclusion: METTL16 promotes cerebral I/R injury by stabilizing TIPARP mRNA via m
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.