ArticleNeuropsychiatric disease and treatment2023
Correlations Between Serum CXCL9/12 and the Severity of Acute Ischemic Stroke, a Retrospective Observational Study.
Article in Neuropsychiatric disease and treatment, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 3 citations in OpenAlex.
- CXCL12/CXCR4 signaling governs ischemic neurovascular pathophysiology and repair: a multidimensional contextual analysis.Angiogenesis · 2026Review
- Circulating Chemokines and Short- and Long-Term Outcomes After Ischemic Stroke.Molecular neurobiology · 2025Article
- Uncovering a new mechanism of ischemic stroke: a study of the association between γδ T cells and immunoinflammation.Frontiers in immunology · 2025Review
- The differential proteomic response to ischemic stroke in appalachian subjects treated with mechanical thrombectomy.Journal of neuroinflammation · 2024Observational
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This retrospective observational study was conducted to determine the correlations between serum CXCL9/12 and the severity of acute ischemic stroke (AIS). Methods: Total 138 patients with AIS were enrolled in the study. These patients underwent Brain CT on admission and blood samples were collected. Serum CXCL9 and CXCL12 were detected by ELISA assay. The correlations of serum CXCL9/12 with AIS was analyzed based on Oxfordshire Community Stroke Project (OCSP) classification, Trial of Org 10,172 in acute stroke treatment (TOAST) classification, National Institutes of Health Stroke Score (NIHSS) score, infarct volume, and modified Rankin scale (mRS) score. Results: Compared with the controls, patients with AIS had higher levels of serum CXCL9 and CXCL12. Logistic regression analysis determined that CXCL9 and CXCL12 were independent risk factors for AIS. In addition, the increased serum CXCL9 and CXCL12 were associated with TOAST classification, NIHSS score, and infarct volume. However, serum CXCL9 and CXCL12 were not associated with functional outcomes (mRS score). CXCL9 and CXCL12 both exhibited a high diagnostic value in AIS. Conclusion: Serum CXCL9 and CXCL12 were elevated in patients with AIS, closely correlated with the severity of AIS.
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Registered trials
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