Endostatin and osteopontin are elevated in patients with both coronary artery disease and aortic valve calcification

Sponder, Michael; Fritzer‐Szekeres, Monika; Litschauer, Brigitte; Binder, Thomas; Strametz-Juranek, Jeanette

doi:10.1016/j.ijcme.2015.08.002

Cited by 8 publications

(7 citation statements)

References 30 publications

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“…Although the mechanism of inducing coronary calcification by ES is not that clear, higher serum ES level associated with valvular calcification was detected in CAD patients. ES was involved in the active process of valvular calcification which is significantly similar to pathogenesis of atherosclerosis [33]. The direct mechanisms related to the serum ES level and calcified atherosclerotic changes may be related to cleavage of ES from collagen XVIII by proteinases [34] such as MMP-9 which has a role in initiation and advancement of atherosclerosis [35], [36].…”

Section: Discussionmentioning

confidence: 97%

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

El-Ashmawy

Roshdy

Saad

et al. 2019

Journal of the Saudi Heart Association

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ObjectiveTo assess the relationship between serum endostatin (ES) and coronary artery calcification (CAC) in type 2 diabetic (T2DM) patients.MethodsThe study included 110 participants with coronary artery disease (CAD); 55 with T2DM, for serum ES levels by enzyme-linked immunosorbent assay and CAC by contrast-enhanced spiral computed tomography (CT).ResultsMean serum ES value was 66.54 ng/mL [95% confidence interval (CI), 61.77–71.32 ng/mL]. Serum ES levels positively correlated with Agatston score index [ASI; r = 0.701, p < 0.001; high sensitive C-reactive protein (hs-CRP) r = 0.783, p < 0.001]. On multiple regression analysis, the highest three ES quartiles (2, 3, and 4) were related to ASI in diabetic patients, adjusted ES level was an independent predictor of CAD [odds ratio (OR) = 1.065; 95% CI, 1.008–1.126; p = 0.026] and for the number of coronary vessels affected (OR = 1.089; 95% CI, 1.018–1.164; p = 0.013) in T2DM patients. Receiver operating characteristics (ROC) analysis showed serum ES at a cutoff value of 86.5 ng/mL can predict the risk of CAC in T2DM, with a sensitivity of 74.1%, specificity of 71.4%, p < 0.001 and area under curve (AUC) of 0.776.ConclusionMeasurement of serum ES levels can improve diagnosis of CAC and could be useful as a high sensitive marker for the presence and progression of atherosclerosis in T2DM patients.

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Section: Discussionmentioning

confidence: 97%

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

El-Ashmawy

Roshdy

Saad

et al. 2019

Journal of the Saudi Heart Association

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“…In contrast, increased serum endostatin levels are found in several cardiovascular associated diseases including CAD, heart failure, diabetes, and hypertension [48]. Specific to CAD, serum endostatin has been shown to be significantly elevated in CAD versus healthy controls, and greater levels of serum endostatin in CAD patients is significantly associated with poorer collateralization, increased disease severity, and a greater risk for future cardiovascular events [39,[49][50][51][52]. Additionally, impairment in endothelial function is significantly associated with increased serum endostatin levels in those with cardiovascular risk factors, such as hypertension [53].…”

Section: Discussionmentioning

confidence: 99%

Endostatin as a Mediator Between Endothelial Function and Cognitive Performance in Those at Risk for Vascular Cognitive Impairment

Isaacs-Trepanier

Saleem

Herrmann

et al. 2020

JAD

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Background: Patients with coronary artery disease have an increased risk for developing vascular cognitive impairment. Endothelial function is often diminished and has been associated with lower cognitive performance in these patients. The link between endothelial function and cognition in coronary artery disease is not fully understood. Angiogenesis may play a role in mediating the association between endothelial function and cognition since angiogenic processes rely heavily on the endothelium. Objective: The aim of this study was to determine if markers of angiogenesis mediate the relationship between endothelial function and cognition in coronary artery disease patients. Methods: In 50 participants with coronary artery disease, endothelial function was assessed using peripheral arterial tonometry. Vascular endothelial growth factor (pro-angiogenic) and endostatin (anti-angiogenic) were measured in peripheral serum samples. Cognition was assessed using the Montreal Cognitive Assessment. A mediation analysis, using a bias corrected inferential bootstrapping method with 10,000 permutations, was used to determine if vascular endothelial growth factor or endostatin mediated an association between peripheral arterial tonometry measures and cognitive performance on the Montreal Cognitive Assessment. Results: Endostatin, but not vascular endothelial growth factor, mediated a relationship between endothelial function and cognitive performance when controlling for total years of education, body mass index, coronary artery bypass graft, stent, diabetes, and diuretic use. This analysis was also significant when delayed recall was substituted for the overall score on the Montreal Cognitive Assessment. Conclusion: These results suggest that endostatin mediates an association between endothelial function and cognitive performance in coronary artery disease.

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“…Calcified valves have been shown to contain small-and medium-sized microvessels as well as organized arterioles. Valve neovascularization is enhanced by the release of proangiogenic factors by inflammatory cells and/or by downregulation of inhibitors of angiogenesis [12]. Mast cells, which contain vascular endothelial growth factor were found to be present and degranulated in calcified valves [13].…”

Section: Immune Responsesmentioning

confidence: 99%

Decellularized tissue-engineered heart valves calcification: what do animal and clinical studies tell us?

Badria

Koutsoukos

Mavrilas

2020

J Mater Sci: Mater Med

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Cardiovascular diseases are the first cause of death worldwide. Among different heart malfunctions, heart valve failure due to calcification is still a challenging problem. While drug-dependent treatment for the early stage calcification could slow down its progression, heart valve replacement is inevitable in the late stages. Currently, heart valve replacements involve mainly two types of substitutes: mechanical and biological heart valves. Despite their significant advantages in restoring the cardiac function, both types of valves suffered from serious drawbacks in the long term. On the one hand, the mechanical one showed non-physiological hemodynamics and the need for the chronic anticoagulation therapy. On the other hand, the biological one showed stenosis and/or regurgitation due to calcification. Nowadays, new promising heart valve substitutes have emerged, known as decellularized tissue-engineered heart valves (dTEHV). Decellularized tissues of different types have been widely tested in bioprosthetic and tissue-engineered valves because of their superior biomechanics, biocompatibility, and biomimetic material composition. Such advantages allow successful cell attachment, growth and function leading finally to a living regenerative valvular tissue in vivo. Yet, there are no comprehensive studies that are covering the performance of dTEHV scaffolds in terms of their efficiency for the calcification problem. In this review article, we sought to answer the question of whether decellularized heart valves calcify or not. Also, which factors make them calcify and which ones lower and/or prevent their calcification. In addition, the review discussed the possible mechanisms for dTEHV calcification in comparison to the calcification in the native and bioprosthetic heart valves. For this purpose, we did a retrospective study for all the published work of decellularized heart valves. Only animal and clinical studies were included in this review. Those animal and clinical studies were further subcategorized into 4 categories for each depending on the effect of decellularization on calcification. Due to the complex nature of calcification in heart valves, other in vitro and in silico studies were not included. Finally, we compared the different results and summed up all the solid findings of whether decellularized heart valves calcify or not. Based on our review, the selection of the proper heart valve tissue sources (no immunological provoking residues), decellularization technique (no damaged exposed residues of the decellularized tissues, no remnants of dead cells, no remnants of decellularizing agents) and implantation techniques (avoiding suturing during the surgical implantation) could provide a perfect anticalcification potential even without in vitro cell seeding or additional scaffold treatment.

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Endostatin and osteopontin are elevated in patients with both coronary artery disease and aortic valve calcification

Cited by 8 publications

References 30 publications

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

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

Endostatin as a Mediator Between Endothelial Function and Cognitive Performance in Those at Risk for Vascular Cognitive Impairment

Decellularized tissue-engineered heart valves calcification: what do animal and clinical studies tell us?

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