ArticleCNS neuroscience & therapeutics2026
Cystatin B Attenuates Cerebral Ischemia Reperfusion Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Oxidative Stress Drives Cell Cycle Stalling, Apoptosis and Metabolic Suppression in Cystatin B Deficient EPM1 Patient iPSCs.Cell proliferation · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundCerebral ischemia reperfusion injury (CIRI) poses a significant clinical and economic burden worldwide. Therefore, it is essential to identify key regulators that may improve stroke prognosis. Cystatin B (CSTB) is known to be involved in neuroprotection, inflammation modulation, and apoptosis regulation, but its specific function and mechanisms in CIRI remain unclear.
methodsWe employed gain- and loss-of-function approaches in a mouse model of transient middle cerebral artery occlusion (t/MCAO) and in cultured neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R). The effects were evaluated primarily using a combination of quantitative PCR, Western blot, and immunofluorescence staining to assess neurological deficits, inflammatory responses, and apoptosis, as well as to elucidate the underlying mechanisms.
resultsOur findings demonstrated that CSTB significantly attenuated CIRI, as evidenced by the mitigation of neurological deficits, inflammation, and apoptosis. Mechanistically, the protective effects of CSTB were associated with the suppression of the JAK2/STAT3 signaling pathway.
conclusionThis study identifies CSTB as a novel negative regulator of CIRI. Its protective role is mediated through the inhibition of apoptosis and inflammatory responses via the JAK2/STAT3 axis, suggesting its potential as a therapeutic target for ischemic stroke.
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Registered trials
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