ArticleCNS neuroscience & therapeutics2025
SFXN1 Reduction Alleviates Cerebral Ischemia-Reperfusion Injury by Promoting Neuronal Survival and Reducing Neuroinflammation.
Article in CNS neuroscience & therapeutics, 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
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
3 citing papers in PubMed.
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- Wuling San ameliorates cerebral ischemia-reperfusion injury via suppression of the TRPM2/NLRP3 pathway.European journal of medical research · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
aimSideroflexin 1 (SFXN1) is an important inner mitochondrial membrane protein that regulates many physiological and pathological events. However, the role of SFXN1 in cerebral ischemia-reperfusion (I/R)-induced neuronal death remains unclear.
methodsWe employed in vivo injury models of transient middle cerebral artery occlusion (tMCAO) and in vitro models of lipopolysaccharide (LPS) stimulation and oxygen-glucose deprivation/reperfusion (OGD/R) to investigate the regulatory effects of SFXN1 on neuroinflammation and brain injury. Western blotting, immunofluorescence, and real-time quantitative PCR were utilized to assess SFXN1 expression, proinflammatory signaling pathways activation, and cytokine levels in vitro. Cerebral infarction was evaluated using 2,3,5-triphenyltetrazolium chloride (TTC) staining and Nissl staining.
resultsSFXN1 expression was upregulated following cerebral I/R injury. Both neurons and microglia exhibited increased SFXN1 expression after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment. SFXN1 knockdown reduced OGD/R-induced neuronal death and alleviated cerebral I/R injury. Additionally, conditioned medium from SFXN1-knockdown microglia reduced neurotoxicity in vitro. Mechanistically, SFXN1 induced mitochondrial dysfunction and neuronal death after OGD/R in an iron-independent manner. Furthermore, SFXN1 promoted the production of proinflammatory cytokines by promoting NF-κB activation, partially through iron transport in microglia after OGD/R.
conclusionThis study reveals the novel role of SFXN1 in exacerbating cerebral I/R injury by reducing neuronal survival through the modulation of mitochondrial function and promotion of microglia-mediated neuroinflammation via NF-κB activation.
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.