Low TGF-β1 serum levels are a risk factor for atherosclerosis disease in ESRD patients

Stefoni, Sergio; Cianciolo, Giuseppe; Donati, Gabriele; Dormi, Ada; Silvestri, Michele; Colì, L.; Pascalis, Antonio De; Iannelli, S.

doi:10.1046/j.1523-1755.2002.00119.x

Cited by 79 publications

(58 citation statements)

References 62 publications

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“…It is secreted in a latent inactive form that is activated proteolytically by plasmin. In turn, plasmin is produced from plasminogen by t-PA, the production of which is blocked by competitive inhibition fron Lp(a) and PAI-1 (Stefoni et al, 2002). Tashiro et al (2002) suggested that plasma concentrations of TGF-b1 decreased in patients with CAD and might have prognostic significance, considering that patients with low levels of TGF-b1 had a significantly poor prognosis in terms of survival.…”

Section: Discussionmentioning

confidence: 99%

Effects of moderate Sicilian red wine consumption on inflammatory biomarkers of atherosclerosis

et al. 2005

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Objective: The aim of the study is to evaluate the effect of moderate Sicilian red wine consumption on cardiovascular risk factors and, in particular, on some inflammatory biomarkers. Methods: A total of 48 subjects of both sexes who were nondrinkers or rare drinkers of moderate red wine were selected and randomly subdivided into two groups assigned to receive with a crossover design a Sicilian red wine (Nero d'Avola or Etna Torrepalino) during meals: Group A (n ¼ 24), in whom the diet was supplemented for 4 weeks with 250 ml/day of red wine, followed by 4 weeks when they returned to their usual wine intake; and Group B (n ¼ 24), in whom the usual wine intake was maintained for 4 weeks, followed by 4 weeks when the diet was supplemented with 250 ml/day of red wine. The following were values measured in all tests: blood glucose, total and HDL-cholesterol and triglycerides, LDL-cholesterol, LDL/HDL ratio, apolipoproteins A1 and B, Lp(a), plasma C-reactive protein, TGFb1, D-Dimer, Factor VII , PAI Ag, t-PA Ag, fibrinogen, oxidized LDL Ab, total plasma antioxidant capacity. Results: At the end of the red wine intake period, LDL/HDL, fibrinogen, factor VII, plasma C-reactive protein and oxidized LDL Ab were significantly decreased, while HDL-C, Apo A1,TGFb1, t-PA, PAI and total plasma antioxidant capacity were significantly increased. Conclusions: Our results show a positive effect of two Sicilian red wines on many risk factors and on some inflammatory biomarkers, suggesting that a moderate consumption of red wine in the adult population is a positive component of the Mediterranean diet.

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Section: Discussionmentioning

confidence: 99%

Effects of moderate Sicilian red wine consumption on inflammatory biomarkers of atherosclerosis

et al. 2005

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“…8,23 -25 Further studies are needed to better understand the pathophysiological mechanisms responsible for elevated Lp(a) levels in HD patients, the pathways responsible for its atherothrombogenic actions, and its possible relationship or interaction with coagulation disorders and inflammatory markers such as cytokines and acutephase proteins. 17,[23][24][25][26] Two wellknown acute-phase proteins, Lp(a) and fibrinogen, were found to increase significantly during a single HD session compared with baseline (pre-HD) values. 17,23 The HD procedure itself has been suggested as a potential source of inflammation.…”

Section: Discussionmentioning

confidence: 97%

“…17 Stefoni et al found that low serum TGF-b1 negatively correlated with Lp(a) and CRP. 24 There is evidence for there being a feedback mechanism between Lp(a) and TGF-b, in which the initial accumulation of Lp(a) particles and purified apo(a) in vessel walls inhibits the local activation of TGF-b, an inhibitor of smooth muscle cell growth, and leads to further accumulation of apo(a) and to smooth muscle proliferation-one of the hallmarks of atherosclerotic lesions. 25 Local inhibition of TGF-b activity by Lp(a) seems to be an initial key, which may partly explain the atherothrombogenic action of Lp(a) and its relation with coagulation disorders that result from smooth muscle cell proliferation and the subsequent lipid accumulation and platelet adhesion to formed lesions, whereas fibrinogen and fibronectin could be the ligands supporting local platelet adhesion and aggregation.…”

Section: Discussionmentioning

confidence: 99%

Relationship between lipoprotein(a), fibrinogen, and fibronectin in non‐diabetic hemodialyzed uremic patients

Tzanatos

Retsa

Soubassi

et al. 2006

Dialysis & Transplantation

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Background. Lipoprotein(a), Lp(a), has been recognized as an atherogenic and thrombogenic lipoprotein in the general population and in hemodialysis (HD) patients. In addition, fibrinogen and fibronectin may promote atherothrombosis. The aim of this study was to investigate any possible relationship between Lp(a) and thrombogenic coagulation proteins in non-diabetic HD patients. Patients and Methods. Serum Lp(a) and plasma fibrinogen, plasminogen, and fibronectin levels were measured pre-HD in 60 uremic patients (30 male, 30 female) aged 58.6 AE 8.0 years who had been receiving HD treatment for 61.3 AE 50.7 months. The control group comprised 20 age-and sex-matched healthy subjects. All patients were receiving erythropoietin treatment. Results. The mean serum Lp(a) (33.88 AE 34.12 mg/dL) and plasma fibrinogen (329.45 AE 80.62 mg/dL) levels were significantly higher in the HD patients compared with those in the controls (16.70 AE 10.36 and 254.00 AE 43.34 mg/dL, respectively; p < .05 and p < .001, respectively). Plasminogen levels did not differ between the HD patients (11.64 AE 3.22 mg/dL) and the control group (10.67 AE 1.41 mg/dL, p>.05). Fibronectin levels were slightly increased in the HD patients (33.96 AE 5.49 mg/dL) versus in the control group (30.9 AE 5.80 mg/dL, p < .05). There was a significant positive correlation between Lp(a) and fibrinogen levels (r ¼ 0.305, p < .02), as well as between Lp(a) and fibronectin levels (r ¼ 0.360, p < .01). Moreover, there was a significant positive correlation between fibrinogen and fibronectin levels (r ¼ 0.587, p < .0001). Conclusions. According to our results, in non-diabetic HD patients, abnormal serum Lp(a) levels significantly correlated with abnormal levels of fibrinogen and fibronectin. There is a concern that the relationship between these atherogenic and thrombogenic acute-phase proteins may contribute to the increased incidence of atherosclerotic cardiovascular disease in this patient population.

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“…Further changes in TGF-␤ activity would result in the formation of both stable and unstable atherosclerotic lesions. 34 It has been proposed that stenotic arteriovenous fistulas can be regarded as a model for accelerated atherosclerosis, 4 and studies in hemodialysis patients have shown that lipoprotein(a) 35 and low TGF-␤1 serum levels 36 are risk factors for atherosclerosis. It is also known that lipoprotein(a) 37 and low shear stress 38 might suppress TGF-␤ activity and that low shear stress also promotes intimal hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

The risk of dialysis access thrombosis is related to the transforming growth factor–β1 production haplotype and is modified by polymorphisms in the plasminogen activator inhibitor–type 1 gene

Lazo‐Langner

Knoll

Wells

et al. 2006

Blood

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Low TGF-β1 serum levels are a risk factor for atherosclerosis disease in ESRD patients

Abstract: TGF-beta1 was significantly reduced in hemodialysis patients, in particular in those with severe cardiovascular disease. Baseline TGF-beta1, diabetes mellitus and serum albumin levels proved to be the only independent contributors to atherosclerotic risk in dialysis patients.

Cited by 79 publications

References 62 publications

Effects of moderate Sicilian red wine consumption on inflammatory biomarkers of atherosclerosis

Effects of moderate Sicilian red wine consumption on inflammatory biomarkers of atherosclerosis

Relationship between lipoprotein(a), fibrinogen, and fibronectin in non‐diabetic hemodialyzed uremic patients

The risk of dialysis access thrombosis is related to the transforming growth factor–β1 production haplotype and is modified by polymorphisms in the plasminogen activator inhibitor–type 1 gene

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