ArticleNeurotoxicity research2026
MicroRNA-132 Alleviates Ischemia-Reperfusion-Induced Neuronal Apoptosis by Targeting Mecp2 in Stroke Models.
Article in Neurotoxicity research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Regulatory mechanisms of post-translational modifications on autophagic flux in neurons following ischemic stroke.Molecular biology reports · 2026Review
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cerebral ischemia-reperfusion injury (CI/RI) remains a significant challenge in ischemic stroke treatment, often leading to exacerbated neuronal apoptosis and poor neurological recovery despite successful recanalization. MicroRNAs (miRNAs) are known to influence neurodegeneration and repair through post-transcriptional modulation of apoptosis-related genes. In this study, we investigated the neuroprotective role of miR-132 and its interaction with the epigenetic regulator Mecp2 under CI/RI conditions. Utilizing a rat MCAO model and SH-SY5Y neuronal cells exposed to OGD/R, we found that miR-132 levels were significantly decreased while Mecp2 expression was elevated following ischemic injury. Functional assays revealed that overexpression of miR-132 restored neuronal viability, increased anti-apoptotic Bcl-2, and reduced pro-apoptotic Bax expression. In contrast, inhibition of miR-132 exacerbated apoptosis. Bioinformatic analysis and dual-luciferase reporter assays confirmed that miR-132 directly targets the 3′UTR of Mecp2. Importantly, Mecp2 overexpression abolished the protective effects of miR-132, indicating that this axis is essential for apoptosis modulation. These findings establish the miR-132/Mecp2 axis as a key determinant of neuronal fate in CI/RI and identify it as a promising target for neuroprotective therapies.
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Registered trials
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