In conclusion, we demonstrate that miR-320/VEGFA axis is crucial to high glucose-induced metabolic memory during HUVEC dysfunction and may be involved in the pathology of diabetes.
Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis and has been investigated as a candidate gene in a number of conditions, including diabetes and its microvascular complications (e.g., retinopathy and nephropathy).
After adjustment for age, gender, duration of diabetes, and BMI, multivariate analysis showed significant association of smoking (<i>p</i>=0.002) and HOMA-IR (<i>p</i>=0.003) with intraocular IL-6 levels, while intraocular VEGF and systemic Lp-A levels correlated significantly (<i>p</i>=0.032).
Oxidative stress is implicated in the development of vascular disease and is associated with an upregulation of vascular endothelial growth factor (VEGF), which is pathogenetically linked to the microvascular complications of diabetes.
Amongst all the DVC, D allele of the VEGF polymorphism had a significantly increased risk of diabetic retinopathy (DR) (OR = 1.31; p = 0.033) irrespective of the duration of diabetes, BMI, the glycemia control expressed by HbA1c, renal function, lipid values or applied treatment.
The present study is the first report to show that cutaneous microangiopathy, as indicated by subepidermal microvascular proliferation and impaired VEGF expression, appears to occur before the development of overt clinical neuropathy, retinopathy or nephropathy in patients with type 2 diabetes.
Intravitreal injections of antibody-based biologics targeting vascular endothelial growth factor (VEGF) are highly effective and have markedly decreased the risk of visual impairment associated with prevalent retinal diseases, such as neovascular age-related macular degeneration and diabetes macular oedema.
Retinal vascular leakage and Müller cell stress as well as vascular endothelial growth factor (VEGF) expression in retina and RPE/choroid, were increased by hypertension or diabetes and there was an additive effect of these conditions.
PF-05231023 administration did not change retinal expression of vascular endothelial growth factor A, suggesting a novel therapeutic approach for the prevention of early diabetic retinopathy by protecting photoreceptor function in diabetes.
Stepwise backward regression analysis showed that GRP78 levels were associated with the VEGF levels and the duration of diabetes (P < .001 and P = .002, respectively).
In conclusion, intravitreal administration of vascular endothelial growth factor inhibitors is unlikely to be associated with a deterioration of renal function in patients with diabetes and chronic kidney disease.
Moreover, quercetin administration progressively increased the expression of vascular endothelial growth factor (VEGF) and its receptor, VEGFR2 in diabetes rats.
Our study concludes that ANRIL regulates functional and structural alterations in the kidneys and hearts in diabetes through controlling the expressions of ECM proteins and VEGF.
After administration of BCA, retina concentrations of vascular endothelial growth factor, tumor necrosis factor-alpha and interleukin-1beta decreased in the 2 groups of treated rats with diabetes compared to the control group with diabetes (p<0.05).
The aim of this study was to investigate the correlation between diabetes-induced testicular damage and testicular VEGF and PARP-1 expression and the possible protective role of vitamin E supplementation.
ALA induced pro-angiogenic effect in the myocardium of rats with diabetes increasing mRNA VEGF expression and decreasing mRNA VEGFR-1 expression, while in the aortal wall ALA increased mRNA VEGFR-2 and VEGFR-1 expression. cVEGF in the ALA-treated group was higher comparing to both control groups.
In this article, I will (1) briefly summarize our work on delineating the role and mechanism of MG-modulated vascular function through the production of vascular endothelial growth factor (VEGF) and on investigating VEGF signaling-mediated MG viability and neural protection in diabetic animal models, (2) explore the relationship among VEGF and neurotrophins in protecting Müller cells in in vitro models of diabetes and hypoxia and its potential implication to neuroprotection in DR and hypoxic retinal diseases, and (3) discuss the relevance of our work to the effectiveness and safety of long-term anti-VEGF therapies, a widely used strategy to combat DR, diabetic macular edema, neovascular age-related macular degeneration, retinopathy of prematurity, and other hypoxic retinal vascular disorders.
Luteolin also inhibited diabetes-induced elevation of interleukin-1 beta (IL-1β), vascular endothelial growth factor and nuclear factor-κB (NF-κB) mRNA and protein expression in lens.
This study was designed to evaluate the protective effect of dasatinib, a potent Src inhibitor used clinically for the treatment of cancer, against the breakdown of the blood-retinal barrier (BRB) and the retinal vascular leakage caused by vascular endothelial growth factor (VEGF) and diabetes.