Vascular endothelial growth factor-mediated peritoneal neoangiogenesis in peritoneal dialysis

2021 ◽  
pp. 089686082110046
Author(s):  
Yingfeng Shi ◽  
Yan Hu ◽  
Binbin Cui ◽  
Shougang Zhuang ◽  
Na Liu
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Peritoneal Dialysis ◽  
Growth Factor ◽  
Vascular Endothelial Cells ◽  
Renal Diseases ◽  
Vascular Endothelial ◽  
Ultrafiltration Failure ◽  
Tumour Growth Factor ◽  
End Stage ◽  
Endothelial Growth Factor

Peritoneal dialysis (PD) is an important renal replacement therapy for patients with end-stage renal diseases, which is limited by peritoneal neoangiogenesis leading to ultrafiltration failure (UFF). Vascular endothelial growth factor (VEGF) and its receptors are key angiogenic factors involved in almost every step of peritoneal neoangiogenesis. Impaired mesothelial cells are the major sources of VEGF in the peritoneum. The expression of VEGF will be up-regulated in specific pathological conditions in PD patients, such as with non-biocompatible peritoneal dialysate, uremia and inflammation, and so on. Other working cells (i.e. vascular endothelial cells, macrophages and adipocytes) can also stimulate the secretion of VEGF. Meanwhile, hypoxia and activation of complement system further aggravate peritoneal injury and contribute to neoangiogenesis. There are several signalling pathways participating in VEGF-mediated peritoneal neoangiogenesis including tumour growth factor-β, Wnt/β-catenin, Notch and interleukin-6/signal transducer and activator of transcription 3. Moreover, VEGF is highly expressed in dialysate effluent of long-term PD patients and is associated with peritoneal transport function, which supports its role in the alteration of peritoneal structure and function. In this review, we systematically summarize the angiogenic effect of VEGF and evaluate it as a potential target for the prevention of peritoneal neoangiogenesis and UFF. Preservation of the peritoneal membrane using targeted therapy of VEGF-mediated peritoneal neoangiogenesis may increase the longevity of the PD modality for those who require life-long dialysis.

scholarly journals The relationship between vascular endothelial growth factor (VEGF) in the serum and drained dialysate with the quality of peritoneal dialysis and peritoneal membrane transport rates

2019 ◽  
Vol 71 (1) ◽  
pp. 187-194
Author(s):  
Natasa Jovanovic ◽  
Snezana Zunic ◽  
Jasna Trbojevic-Stankovic ◽  
Zeljko Lausevic ◽  
Dejan Nesic ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Peritoneal Dialysis ◽  
Growth Factor ◽  
Residual Renal Function ◽  
Vascular Endothelial ◽  
Peritoneal Membrane ◽  
Equilibrium Test ◽  
End Stage ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF), a powerful angiogenetic agent crucial for microvascular hyperpermeability and neoangiogenesis in the peritoneum, is associated with increased solute transport rates in chronic peritoneal dialysis (PD) patients. We investigated the correlation between serum and drained dialysate (dd) concentrations of VEGF and the transport characteristics of peritoneal membrane and dialysis quality in 20 patients with end-stage renal failure at the beginning and after six months of PD. The serum VEGF (sVEGF) concentration rose significantly (149.33?}116.71 pg/ mL vs 239.36?}102.23 pg/mL; p=0.012) and ddVEGF concentration increased slightly (38.44?}50.47 pg/mL vs 43.55?}51.10 pg/mL) during the first 6 months of PD. At the beginning of chronic PD, ddVEGF concentrations correlated inversely with the peritoneal equilibrium test (PET) glucose (R=-0.565; p=0.009) and creatinine (R=-0.506; p=0.023) and residual renal function (RRF) (R=-0.691; p=0.001); sVEGF concentrations inversely correlated with PET creatinine (R=-0.457; p=0.043) and residual diuresis (RD) (R=-0.691; p=0.001). After 6 months of treatment, ddVEGF concentrations correlated directly with PETcreatinine (R=0.450; p=0.047), and inversely with RRF (R=-0.552; p=0.012) and residual renal weekly Kt/V (R=-0.488; p=0.029). The sVEGF concentration inversely correlated with RD (R=-0.589; p=0.006). High ddVEGF at the beginning of PD is predictive of adverse alterations of the peritoneal membrane, i.e. increased transport rate of glucose and creatinine. ddVEGF values may help to identify patients who will preserve adequate transport characteristics of the peritoneal membrane and maintain successful long-term PD.

scholarly journals Nephrotoxicity induced by vascular endothelial growth factor inhibitors

2021 ◽  
Vol 11 (1) ◽  
pp. e4-e4
Author(s):  
Shirinsadat Badri ◽  
Lillian Siberian ◽  
Rasool Soltani ◽  
Azadeh Moghaddas ◽  
Sara Ataei ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Kinase Inhibitor ◽  
Vascular Endothelial Cells ◽  
Angiogenesis Inhibitors ◽  
Renal Diseases ◽  
Vascular Endothelial ◽  
Vegf Receptors ◽  
Vegf Inhibitors ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a special mitogen for vascular endothelial cells, an essential endogenous angiogenic cytokine, and the principal controller of vascular growth that plays a fundamental role in therapeutic angiogenesis pathways. VEGF-targeted therapy is categorized into the group of angiogenesis inhibitors that inhibit the expression or the activity of VEGF. It comprises counteracting VEGF antibodies, VEGF receptors, VEGF-trap, and tyrosine kinase inhibitor (TKIs) with selectivity for VEGF receptors. The kidney is both a target and a source of VEGF. VEGF may be a vital mediator to restore some types of renal diseases (e.g., non-diabetic renal diseases) and harmful in some other diseases (e.g., diabetes and diabetes complications). Due to their ability to prevent angiogenesis, VEGF inhibitors have been found as a powerful tool to treat angiogenesis-dependent diseases, including cancer and diabetic retinopathy. VEGF preserves the renal structure and function in normal physiologic conditions. Therefore, all treatments that inhibit the VEGF pathway may lead to renal disorders, especially renovascular diseases such as hypertension, proteinuria, nephrotic syndrome, decreased glomerular filtration rate (GFR), and thrombotic microangiopathy (TMA). In the present study, we reviewed some related reports and associated mechanisms, especially for hypertension and proteinuria.

scholarly journals Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

2000 ◽  
Vol 74 (22) ◽  
pp. 10699-10706 ◽  
Author(s):  
Loreen J. Savory ◽  
Steven A. Stacker ◽  
Stephen B. Fleming ◽  
Brian E. Niven ◽  
Andrew A. Mercer
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Virus Infection ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Skin Lesions ◽  
Orf Virus ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

ABSTRACT Infection by the parapoxvirus orf virus causes proliferative skin lesions in which extensive capillary proliferation and dilation are prominent histological features. This infective phenotype may be linked to a unique virus-encoded factor, a distinctive new member of the vascular endothelial growth factor (VEGF) family of molecules. We constructed a recombinant orf virus in which the VEGF-like gene was disrupted and show that inactivation of this gene resulted in the loss of three VEGF activities expressed by the parent virus: mitogenesis of vascular endothelial cells, induction of vascular permeability, and activation of VEGF receptor 2. We used the recombinant orf virus to assess the contribution of the viral VEGF to the vascular response seen during orf virus infection of skin. Our results demonstrate that the viral VEGF, while recognizing a unique profile of the known VEGF receptors (receptor 2 and neuropilin 1), is able to stimulate a striking proliferation of blood vessels in the dermis underlying the site of infection. Furthermore, the data demonstrate that the viral VEGF participates in promoting a distinctive pattern of epidermal proliferation. Loss of a functional viral VEGF resulted in lesions with markedly reduced clinical indications of infection. However, viral replication in the early stages of infection was not impaired, and only at later times did it appear that replication of the recombinant virus might be reduced.

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