ArticleMolecular neurobiology2025
B355252 Targets UCP2 to Rescue Intracerebral Hemorrhage-Induced Injury by Promoting Mitochondrial Fusion and Inhibiting Ferroptosis.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ferroptosis in intracerebral hemorrhage: a bibliometric overview of mechanisms and future directions.Frontiers in cellular neuroscience · 2026Pooled it
- Organelle regulation of ferroptosis after intracerebral hemorrhage.Redox biology · 2026Review
- Mitochondrial dysfunction in intracerebral hemorrhage: molecular mechanisms and pathological consequences.Frontiers in cellular neuroscience · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Intracerebral hemorrhage (ICH), a subtype of stroke, is associated with extremely high mortality and disability rates. The small-molecule compound B355252 exhibits neuroprotective effects against oxidative stress and ferroptosis. However, whether B355252 exerts protective effects against ICH-induced injury remains undefined. Furthermore, the therapeutic time window of B355252 for ICH has not been systematically elucidated. Therefore, this study aims to investigate the therapeutic effects of B355252 on ICH, elucidate its role and underlying mechanisms in inhibiting ICH progression, and determine its therapeutic time window. In this study, a mouse model of collagenase-induced intracerebral hemorrhage was established. Multifaceted assessments included histopathological analysis, behavioral tests, transmission electron microscopy (TEM), and lipid peroxidation assays. Results showed that B355252 significantly reduced the hematoma volume and improved neurological deficits in ICH mice. Mechanically, B355252 regulated mitochondrial dynamics and enhanced mitochondrial structural integrity by targeting uncoupling protein 2 (UCP2), leading to upregulation of the fusion protein MFN2 and inhibition of the fission protein FIS1. In addition, B355252 significantly inhibited oxidative stress by maintaining mitochondrial homeostasis, thereby reducing lipid peroxidation and alleviating ferroptosis. Notably, safety assessment confirmed no organ toxicity and extended the treatment time window to 8.5 h. In conclusion, B355252 is a novel UCP2 agonist that maintains mitochondrial function by regulating mitochondrial dynamics and inhibits ferroptosis by mitigating oxidative stress. It overcomes the critical 6-h treatment time window limitation in the ICH model, paving the way for novel research directions in ICH treatment.
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Registered trials
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