Serum endostatin level as a marker for coronary artery calcification in type 2 diabetic patients

El-Ashmawy, Hazem M.; Roshdy, Hisham Samir; Saad, Zizi; Ahmed, Azza M.

doi:10.1016/j.jsha.2018.09.001

Cited by 5 publications

(4 citation statements)

References 40 publications

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“…Col18a1 may give rise to endostatin by proteolytic splicing. Serum endostatin levels are elevated in coronary artery disease, and have been reported as a sensitive marker for improved coronary artery calcification diagnosis and follow-up [29,30]. Interestingly, Col12a1 was the only protein from the collagen family, which was significantly downregulated in our model.…”

Section: Discussionmentioning

confidence: 70%

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Bergh

Moudt

Branden

et al. 2021

IJMS

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Arterial media calcification (AMC) is predominantly regulated by vascular smooth muscle cells (VSMCs), which transdifferentiate into pro-calcifying cells. In contrast, there is little evidence for endothelial cells playing a role in the disease. The current study investigates cellular functioning and molecular pathways underlying AMC, respectively by, an ex vivo isometric organ bath set-up to explore the interaction between VSMCs and ECs and quantitative proteomics followed by functional pathway interpretation. AMC development, which was induced in mice by dietary warfarin administration, was proved by positive Von Kossa staining and a significantly increased calcium content in the aorta compared to that of control mice. The ex vivo organ bath set-up showed calcified aortic segments to be significantly more sensitive to phenylephrine induced contraction, compared to control segments. This, together with the fact that calcified segments as compared to control segments, showed a significantly smaller contraction in the absence of extracellular calcium, argues for a reduced basal NO production in the calcified segments. Moreover, proteomic data revealed a reduced eNOS activation to be part of the vascular calcification process. In summary, this study identifies a poor endothelial function, next to classic pro-calcifying stimuli, as a possible initiator of arterial calcification.

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Section: Discussionmentioning

confidence: 70%

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Bergh

Moudt

Branden

et al. 2021

IJMS

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“…It has been hypothesized that angiostatin upregulated levels correlate significantly with reduced angiogenesis and poorly developed cardiac collateral vasculature [28]. The most recent study of ElAshmawy et al [29] has demonstrated that elevated levels of another angiogenesis suppressor, endostatin, are associated with coronary artery calcification in type 2 diabetic patients. In our previous studies, we have shown the possibility of pharmacological targeting of circulating angiosta-tin levels by Larginine and simvastatin in patients with coronary heart disease and chronic heart failure [30,31].…”

Section: Fig 1 Cytidine Diphosphate-choline (Cdp-choline or Citicomentioning

confidence: 99%

Citicoline affects serum angiostatin and neurospecific protein levels in patients with atrial fibrillation and ischemic stroke

Tykhomyrov¹,

Kushnir²,

Nedzvetsky³

et al. 2019

Ukr.Biochem.J.

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Ischemic stroke is considered as one of the most frequent and severe complications of atrial fibrillation. The present study was undertaken to examine whether post-insult treatment with cytidine diphosphate-choline (CDP-choline, or citicoline) affects serum levels of the angiogenesis inhibitor angiostatin and neurospecific proteins as markers of brain damage in patients with cerebral ischemia associated with atrial fibrillation. Thirty-three patients with a diagnosis of acute ischemic stroke received citicoline sodium by intravenous infusions (1,000 mg daily for 14 days) in addition to the standard treatment (basic group). Twentyfive patients with the same pathologies, who received only standard therapy, were enrolled in the study as a control group. Serum content of angiostatin and neurospecific proteins, namely neurofilament heavy subunit (NF-H) and glial fibrillary acidic protein (GFAP), was measured by immunoblotting at the basal level and after the treatment. Citicoline treatment caused significant decreases in serum levels of angiostatin (by 40% vs. basal level, P < 0.05), GFAP (by 61%, P < 0.01), and the NF-H subunit (by 19%, P < 0.05) and had no effect on the serum albumin content. In contrast, there were no statistically significant differences between baseline levels of the studied protein markers and their content after the treatment period in the control group. These findings indicate for the first time that CDP-choline protects both astrocytes and neurons and improves angiogenic capacity through down-regulation of angiostatin in post-ischemic patients with atrial fibrillation after acute ischemic stroke. Further studies are needed to test associations between serum levels of these biomarkers, clinical outcomes, and treatment efficacy of stroke. K e y w o r d s: atrial fibrillation, ischemic stroke, citicoline, angiostatin, neurofilaments (NFs), glial fibrillary acidic protein (GFAP).I schemic stroke is a complex multifactorial and polygenic disease. It is generally accepted that one of the major risk factors for ischemic stroke is atrial fibrillation [1]. Past studies indicate that fibrillation of the atrium produces stasis of blood, which causes thrombus formation and embolism in the brain [2,3]. More recent investigations suggest that the pathogenesis of stroke in atrial fibrillation is more complicated and involves other factors in addition to the dysrhythmia [4,5]. It is well acknowled ged that atrial fibrillation is the most prevalent car-diac arrhythmia, affecting approximately 12% of the population worldwide. Being an independent risk factor for stroke, atrial fibrillation is associated with high mortality, morbidity, and socioeconomic burden [6]. Therefore, stroke prevention with appropriate prophylaxis remains central to management of both atrial fibrillation and its neurological complications. However, the search for effective neuroprotectors remains frustrating, and the current therapeutic protocols remain suboptimal. Ideally, sufficient protection must be provided to the ischemic brain a...

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“…[ 1 , 2 ] At present, it is generally believed that coronary artery calcification (CAC) is a predetermined marker of subclinical atherosclerosis and an independent predictor of coronary artery disease. [ 3 , 4 ] CAC is closely related to atherosclerotic plaque load and cardiovascular event incidence. Calcification usually occurs in the early stages of atherosclerosis, but the initial symptoms of calcification are not obvious.…”

Section: Introductionmentioning

confidence: 99%

“…It is mainly caused by coronary atherosclerosis, which causes blockage or stenosis of blood vessels, ischemia and hypoxia of myocardium, and even myocardial necrosis [1,2] . At present, it is generally believed that coronary artery calcification (CAC) is a predetermined marker of subclinical atherosclerosis and an independent predictor of coronary artery disease [3,4] . CAC is closely related to atherosclerotic plaque load and cardiovascular event incidence.…”

Section: Introductionmentioning

confidence: 99%

Association of cystatin C with coronary artery calcification in patients undergoing multidetector computed tomography

Xiong¹,

Wang²,

Jin³

et al. 2021

Medicine

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Cystatin C is associated with atherosclerosis, but the relationship between cystatin C and coronary artery calcification (CAC) is uncertain. The purpose of this study was to evaluate the predictive value of cystatin C on the occurrence and severity of CAC.A total of 1447 hospitalized patients with coronary computed tomography angiography were selected in this study. According to the CAC score (CACS), patients were divided into calcification group (with CAC, n = 749) and control group (without CAC, n = 698). The calcification group was further divided into low calcification group (CACS < 100, n = 407), medium calcification group (CACS 100-400, n = 203), and high calcification group (CACS≥400, n = 139).Patients with CAC had higher cystatin C level than those in control group (P < .05). With the increase of calcification score, the cystatin C level showed an upward trend. The cystatin C level in the high calcification group was significantly higher than those in the low and medium calcification group (P < .05). ROC curve analysis showed that cystatin C had a high predictive value for the occurrence of CAC [area under the curve 0.640, 95% confidence interval (95% CI) 0.591-0.690, cut-off value 0.945 mg/L, sensitivity 0.683, specificity 0.558, P < .05] and severe CAC (area under the curve 0.638, 95% CI 0.550-0.762, cut-off value 0.965 mg/L, sensitivity 0.865, specificity 0.398, P < .05). Multivariate logistic regression analysis showed that cystatin C was an independent predictor of severe CAC (AOR 3.748, 95% CI 1.138-10.044, P < .05).Cystatin C was significantly associated with the occurrence and severity of CAC, suggesting that cystatin C had the potential as a predictor of CAC. Abbreviations: AOR = adjusted odd ratio, CAC = coronary artery calcification, CACS = coronary artery calcification score, CI = confidence interval, CysC = Cystatin C, eGFR = estimated glomerular filtration rate, IL-6 = interleukin-6, LAD = left anterior descending, LCX = circumflex, LM = left main, MDRD = modification of diet in renal disease trial, OPG = osteoprotegerin, p38MAPK = p38 mitogen-activated protein kinase, RANK = receptor activator of nuclear factor-kB, RANKL = RANK ligand, RCA = right coronary artery, ROC = receiver operating characteristic, TNF-a = tumor necrosis factor-a.

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Serum endostatin level as a marker for coronary artery calcification in type 2 diabetic patients

Cited by 5 publications

References 40 publications

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Citicoline affects serum angiostatin and neurospecific protein levels in patients with atrial fibrillation and ischemic stroke

Association of cystatin C with coronary artery calcification in patients undergoing multidetector computed tomography

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