Future clinical and translational research should address whether molecular regulation of VEGF-A pre-mRNA splicing might represent a potential therapeutic strategy for the SSc-related peripheral vasculopathy and, most widely, for other pathologic conditions in humans in which we seek to promote or inhibit angiogenesis.
Decreased cathepsin V expression due to Fli1 deficiency contributes to the development of dermal fibrosis and proliferative vasculopathy in systemic sclerosis.
Overall, miRNA-dependent crosstalk between Ang-2 and VEGF plays a role in hypoxia-induced microvascular response. miRNA-based therapy can affect the expression of Ang-2 and VEGF, which represents a therapeutic potential for the treatment of vascular disease.
Mean serum ACE level was significantly higher in the lupus nephritis and SLE patients with vasculopathy compared with controls (p = 0.008, p = 0.001, respectively).
The underlying angiopathy is characterized by a unique type of ultrastructural basal lamina deposits and by degeneration of vascular smooth muscle cells which are the major source of Notch3 expression.
S1P bound to albumin, but not to apoM, induces PAI-1 expression in adipocytes, indicating that S1P can exert different properties on the pathogenesis of vascular diseases, depending on its vehicle.
Induction of endothelial nitric oxide synthase expression by IL-17 in human vascular endothelial cells: implications for vascular remodeling in transplant vasculopathy.
Endothelial cell expression of interleukin-6 messenger RNA (1.94 +/- 0.24 vs 1.31 +/- 0.16) and interleukin-8 messenger RNA (2.62 +/- 0.33 vs 1.64 +/- 0.22) were enhanced in response to incubation with fetal plasma from placental vascular disease in comparison to incubation with fetal plasma from normal pregnancy.
In conclusion, DMF prevented abnormal proliferation in VSMCs by G1 cell cycle arrest via p21 upregulation driven by Nrf2 and p53 activity, and had a beneficial effect on TNF-α-induced apoptosis and dysfunction in endothelial cells through Nrf2-NQO1 activity suggesting that DMF might be a therapeutic drug for patients with vascular disease.
In the microcirculation of the placenta, endothelial cell expression of interleukin-6 messenger RNA (2.50+/-0.60 vs 1.25+/-0.26) and interleukin-8 messenger RNA (2.83+/-0.55 vs 1.58+/-0.27) was up-regulated in umbilical placental vascular disease in comparison to normal pregnancy.
In conclusion, DMF prevented abnormal proliferation in VSMCs by G1 cell cycle arrest via p21 upregulation driven by Nrf2 and p53 activity, and had a beneficial effect on TNF-α-induced apoptosis and dysfunction in endothelial cells through Nrf2-NQO1 activity suggesting that DMF might be a therapeutic drug for patients with vascular disease.
The purpose of this study was to examine arterial wall expression of the plasminogen activation system in coronary arteries during graft vascular disease initiation and progression.
PPARgamma activation in human endothelial cells increases plasminogen activator inhibitor type-1 expression: PPARgamma as a potential mediator in vascular disease.
Early studies on patients with vascular disease described elevated Hcy concentrations after methionine loading and decreased CBS activity, resembling heterozygotes for CBS deficiency.
Using transgenic mice with mineralocorticoid receptor expression specifically modulated in endothelial cells, recent studies support the emerging concept that while endothelial cell mineralocorticoid receptor may be protective in health, in the presence of CRFs, endothelial cell mineralocorticoid receptor activity contributes to endothelial dysfunction and progression of vascular disease.
Explanations for familial stroke aggregation include differential phenotypic expression of apolipoprotein (a) and apolipoprotein E, racial variations in the distribution of vascular disease, identification of the autosomal-dominant disorder cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, specific point mutations in the mitochondrial-related disorders, and identification of the clinical significance of hereditable coagulopathies.
NADPH oxidases of the Nox family are differentially expressed in the cardiovascular system, induced or activated by cardiovascular risk factors and importantly contribute to the oxidative burden of vascular diseases.