ArticleInternal and emergency medicine2015
FGF-23 levels in patients with critical carotid artery stenosis.
Article in Internal and emergency medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- FGF-23 as a Biomarker for Carotid Plaque Vulnerability: A Systematic Review.Medical sciences (Basel, Switzerland) · 2025Pooled it
- Relationship between fibroblast growth factor in plasma and carotid plaque neovascularization: a pilot study.Frontiers in immunology · 2024Article
- Current Biomarkers for Carotid Artery Stenosis: A Comprehensive Review of the Literature.Metabolites · 2023Review
- Perioperative variation in serum FGF-23 level and its correlation with MACCE risk in unprotected left main coronary artery disease patients receiving coronary artery bypassing grafting.Frontiers in surgery · 2022Article
- Mitochondrial C5aR1 activity in macrophages controls IL-1β production underlying sterile inflammation.Science immunology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to evaluate fibroblast growth factor (FGF)-23 serum levels and its tissue expression in patients with critical carotid artery stenosis (CAS). We selected 35 patients with critical CAS undergoing carotid thromboendoarterectomy. In each patient, FGF-23 serum levels were evaluated just prior to the surgery (t0) and 30 min (t1) thereafter. Moreover, macrophage cytokines were measured at baselines. Carotid artery specimens were used for immune histochemistry. On the basis of the histology, the patients were divided into 2 groups: A with complicated plaque and B with uncomplicated plaque. Twenty complicated plaques (57.14%, group A,) and 15 uncomplicated (42.86%, group B) were evaluated: calcifications were present in 16/20 (80%) complicated plaques and in 6/15 (40%) uncomplicated plaques. An inflammatory infiltrate was observed in 26/35 carotid samples: 18/26 (69.23%) complicated and 8/26 (30.76%) uncomplicated. FGF-23(+) cells were present in 17/20 complicated (85%) and in 8 uncomplicated (53%) plaques. The double-staining immunofluorescence confirmed that macrophage cells (CD68(+)) were also positive for FGF-23 staining. Serum levels of FGF-23 were significantly higher in group A versus group B at t0 (p < 0.05) and t1 (p 0.0047). Moreover, in group A patients a significant increase of FGF-23 serum levels was observed at t1 in comparison with t0 (p 0.0011). Our results suggest that FGF-23 acts in the late phases of atherosclerotic disease and may potentially represent a marker of complications in critical CAS.
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