Increased expression of TGF-β1 and IGF-I in inflammatory stenotic lesions of hemodialysis fistulas

Stracke, Sylvia; Könner, Klaus; Köstlin, Isabella; Friedl, Reinhard; Jehle, Peter; Hombach, Vinzenz; Keller, Frieder; Waltenberger, Johannes

doi:10.1046/j.1523-1755.2002.00191.x

Cited by 119 publications

(121 citation statements)

References 36 publications

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“…TGF-b1 and IGF-I were found to work in concert in regulating the activity of an oestrogen-metabolising enzyme called estradiol-17-b hydroxysteroid dehydrogenase in MCF-7 cells (Wong et al, 2001). Jointly elevated TGF-b1 and IGF-I were also seen in sera and local tissues under other pathological conditions (Li et al, 2002;Stracke et al, 2002). Thus, our finding of positive correlations between TGF-b1 and IGFs in breast cancer does not seem to be unexpected, and it may have some biologic implications in the disease.…”

Section: Discussionsupporting

confidence: 50%

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Katsaros

et al. 2008

Br J Cancer

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Transforming growth factor-b (TGF-b)-mediated signals play complicated roles in the development and progression of breast tumour. The purposes of this study were to analyse the genotype of TGF-b1 at T29C and TGF-b1 phenotype in breast tumours, and to evaluate their associations with IGFs and clinical characteristics of breast cancer. Fresh tumour samples were collected from 348 breast cancer patients. TGF-b1 genotype and phenotype were analysed with TaqMan s and ELISA, respectively. Members of the IGF family in tumour tissue were measured with ELISA. Cox proportional hazards regression analysis was performed to assess the association of TGF-b1 and disease outcomes. Patients with the T/T (29%) genotype at T29C had the highest TGF-b1, 707.9 pg mg À1 , followed by the T/C (49%), 657.8 pg mg À1 , and C/C (22%) genotypes, 640.8 pg mg À1 , (P ¼ 0.210, T/T vs C/C and C/T). TGF-b1 concentrations were positively correlated with levels of oestrogen receptor, IGF-I, IGF-II and IGFBP-3. Survival analysis showed TGF-b1 associated with disease progression, but the association differed by disease stage. For early-stage disease, patients with the T/T genotype or high TGF-b1 had shorter overall survival compared to those without T/T or with low TGF-b1; the hazard ratios (HR) were 3.54 (95% CI: 1.21 -10.40) for genotype and 2.54 (95% CI: 1.10 -5.89) for phenotype after adjusting for age, grade, histotype and receptor status. For late-stage disease, however, the association was different. The T/T genotype was associated with lower risk of disease recurrence (HR ¼ 0.13, 95% CI: 0.02 -1.00), whereas no association was found between TGF-b1 phenotype and survival outcomes. The study suggests a complex role of TGF-b1 in breast cancer progression, which supports the finding of in vitro studies that TGF-b1 has conflicting effects on tumour growth and metastasis.

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Section: Discussionsupporting

confidence: 50%

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Katsaros

et al. 2008

Br J Cancer

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“…Stenotic fistula and graft lesions are associated with profibrotic cytokine production, local inflammation, and neointimal proliferation. 17,18 Repeated trauma at venipuncture sites and turbulent blood flow may promote this process. Most access problems in our study were related to stenosis or thrombosis, supporting this theory.…”

Section: Discussionmentioning

confidence: 99%

Risk of Vascular Access Complications with Frequent Hemodialysis

Suri

Larive

Sherer

et al. 2013

Journal of the American Society of Nephrology

151

110

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Frequent hemodialysis requires using the vascular access more often than with conventional hemodialysis, but whether this increases the risk for access-related complications is unknown. In two separate trials, we randomly assigned 245 patients to receive in-center daily hemodialysis (6 days per week) or conventional hemodialysis (3 days per week) and 87 patients to receive home nocturnal hemodialysis (6 nights per week) or conventional hemodialysis, for 12 months. The primary vascular access outcome was time to first access event (repair, loss, or access-related hospitalization). Secondary outcomes were time to all repairs and time to all losses. In the Daily Trial, 77 (31%) of 245 patients had a primary outcome event: 33 repairs and 15 losses in the daily group and 17 repairs, 11 losses, and 1 hospitalization in the conventional group. Overall, the risk for a first access event was 76% higher with daily hemodialysis than with conventional hemodialysis (hazard ratio [HR], 1.76; 95% confidence interval [CI], 1.11-2.79; P=0.017); among the 198 patients with an arteriovenous (AV) access at randomization, the risk was 90% higher with daily hemodialysis (HR, 1.90; 95% CI, 1.11-3.25; P=0.02). Daily hemodialysis patients had significantly more total AV access repairs than conventional hemodialysis patients (P=0.011), with 55% of all repairs involving thrombectomy or surgical revision. Losses of AV access did not differ between groups (P=0.58). We observed similar trends in the Nocturnal Trial, although the results were not statistically significant. In conclusion, frequent hemodialysis increases the risk of vascular access complications. The nature of the AV access repairs suggests that this risk likely results from increased hemodialysis frequency rather than heightened surveillance.

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“…Recent work also documents a high incidence of inflow arterial stenosis (11). Stenosed AVF have been shown to have venous neointimal hyperplasia composed of smooth muscle cells with expression of cytokines and mediators such as endothelin, PDGF, and TGF-␤ (the last has been shown to co-localize with markers of oxidative stress) within the media and intima (12,13).…”

Section: Pathology Of Native Fistula and Ptfe Graft Failurementioning

confidence: 99%

Hemodialysis Vascular Access Dysfunction

Roy‐Chaudhury

Sukhatme

Cheung³

2006

Journal of the American Society of Nephrology

505

283

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Hemodialysis vascular access dysfunction is a major cause of morbidity and hospitalization in the hemodialysis population. The major cause of hemodialysis vascular access dysfunction is venous stenosis as a result of neointimal hyperplasia. Despite the magnitude of the clinical problem, however, there has been a paucity of novel therapeutic interventions in this field. This is in marked contrast to a recent plethora of targeted interventions for the treatment of arterial neointimal hyperplasia after coronary angioplasty. The reasons for this are two-fold. First there has been a relative lack of cellular and molecular research that focuses on venous neointimal hyperplasia in the specific setting of hemodialysis vascular access. Second, there have been inadequate efforts by the nephrology community to translate the recent advances in molecular and interventional cardiology into therapies for hemodialysis vascular access. This review therefore (1) briefly examines the different forms of hemodialysis vascular access that are available, (2) describes the pathology and pathogenesis of hemodialysis vascular access dysfunction in both polytetrafluoroethylene grafts and native arteriovenous fistulae, (3) reviews recent concepts about the pathogenesis of vascular stenosis that could potentially be applied in the setting of hemodialysis vascular access dysfunction, (4) summarizes novel experimental and clinical therapies that could potentially be used in the setting of hemodialysis vascular access dysfunction, and, finally, (5) offers some broad guidelines for future innovative translational and clinical research in this area that hopefully will reduce the huge clinical morbidity and economic costs that are associated with this condition.

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Increased expression of TGF-β1 and IGF-I in inflammatory stenotic lesions of hemodialysis fistulas

Cited by 119 publications

References 36 publications

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Risk of Vascular Access Complications with Frequent Hemodialysis

Hemodialysis Vascular Access Dysfunction

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