FGF-23 levels in patients with critical carotid artery stenosis

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.

Mitochondrial C5aR1 activity in macrophages controls IL-1β production underlying sterile inflammation

“…7D). Treatment with either the cell-permeable or non–cell-permeable C5aR1 inhibitor reduced the production of fibroblast growth factor (FGF), a hallmark growth factor of macrophages in advanced atherosclerotic lesions ( 48 , 49 ). This observation may indicate that the surface C5aR1 activity of macrophages in plaques serves a specific function connected to FGF biology (fig.…”

Relationship between fibroblast growth factor in plasma and carotid plaque neovascularization: a pilot study

“…Moreover, Del Porto et al. detected FGF-23 inside the atherosclerotic plaque after endarterectomy and plaque immunohistochemistry ( 22 ).…”

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

“…The present study found that the preoperative FGF-23 level was independently correlated with a higher cumulating MACCE rate; meanwhile, the FGF-23 level at discharge showed a trend to be positively associated with the cumulative MACCE rate but did not reach statistical significance. The possible explanations could be that FGF-23 might facilitate the progression of atherosclerosis through several methods including regulating oxidative stress and proliferation of vascular endothelial cells, as well as promoting the infiltration of macrophages ( 18 , 20 , 25 , 26 ). Therefore, preoperative FGF-23 could directly induce the incidence of MACCE.…”