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diabetic angiopathies/phosphatase
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Diabetic hepatosclerosis: diabetic microangiopathy of the liver.
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BACKGROUND
Liver disease associated with diabetes mellitus is common and usually takes the form of simple steatosis or nonalcoholic steatohepatitis. After observing a noncirrhotic form of hepatic sinusoidal fibrosis in patients with long-standing diabetes mellitus who underwent liver biopsy, we set
Exenatide can inhibit calcification of human VSMCs through the NF-kappaB/RANKL signaling pathway.
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BACKGROUND
Arterial calcification is an important pathological change of diabetic vascular complication. Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) plays an important cytopathologic role in arterial calcification. The glucagon-like peptide-1 receptor agonists (GLP-1RA), a
The effect of zipper-interacting protein kinase on high glucose-stimulated human aortic smooth muscle cells.
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Biologic abnormalities in vascular smooth muscle cells (VSMC) may perform a crucial role in the pathogenesis of diabetic vascular disease. The principal aim of this study was to determine the effects of zipper-interacting protein kinase (ZIPK) on human aortic smooth muscle cells (HASMCs) stimulated
Advanced glycation end product Nε-carboxymethyllysine induces endothelial cell injury: the involvement of SHP-1-regulated VEGFR-2 dephosphorylation.
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N(ε)-carboxymethyllysine (CML), a major advanced glycation end product, plays a crucial role in diabetes-induced vascular injury. The roles of protein tyrosine phosphatases and vascular endothelial growth factor (VEGF) receptors in CML-related endothelial cell injury are still unclear. Human
Alterations of glycosaminoglycan metabolism in the development of diabetic complications in relation to metabolic control.
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Disturbed metabolism of glycosaminoglycans (GAGs) has been proposed to play an important role in the pathogenesis of late diabetic complications. The effect of diabetic complications and metabolic control on both total serum GAGs content and the serum activity of lysosomal glycosidases
Activities of Lysosomal Enzymes in Alloxan-Induced Diabetes in the Mouse.
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The study investigated a panel of lysosomal enzymes in the liver and kidney tissues in alloxan-induced diabetes in the mouse. The mice were divided into six experimental groups receiving 10% alloxan at a dose of 50 and 75 mg/kg over a period of four, eight, and twelve days; each group was compared
[Microalbuminuria as a risk factor for diabetic osteopathy in patients with IDDM and renal sufficiency].
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Disturbances in bone marrow vascularisation can be one of the causes of diabetic osteopathy. The aim of the study was to answers the question if microalbuminuria as a results of capillary injury can be a sign of bone mineralisation disorders in IDDM renal sufficient patients. We examined 60 IDDM
Nε-carboxymethyllysine-mediated endoplasmic reticulum stress promotes endothelial cell injury through Nox4/MKP-3 interaction.
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N(ε)-carboxymethyllysine (CML) is an important driver of diabetic vascular complications and endothelial cell dysfunction. However, how CML dictates specific cellular responses and the roles of protein tyrosine phosphatases and ERK phosphorylation remain unclear. We examined whether endoplasmic
Diabetic hepatosclerosis: another diabetes microvascular complication?
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BACKGROUND
Liver disease in diabetes is common and is frequently the result of hepatic steatosis. Diabetic hepatosclerosis is a relatively recent description of sinusoidal fibrosis, without steatosis, observed in liver biopsies of people with diabetes presenting with cholestasis. Its association
Increasing neutrophil F-actin corrects CD11b exposure in Type 2 diabetes.
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BACKGROUND
Leukocyte dysfunction contributes to the pathogenesis of diabetic vascular complications. Neutrophils adhere to the endothelium through the beta(2)integrin CD11b/CD18. In Type 2 diabetes, neutrophil surface CD11b expression is increased and is associated with impaired actin
PP2A contributes to endothelial death in high glucose: inhibition by benfotiamine.
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Endothelial death is critical in diabetic vascular diseases, but regulating factors have been only partially elucidated. Phosphatases play important regulatory roles in cell metabolism, but have not previously been implicated in hyperglycemia-induced cell death. We investigated the role of the
Downregulation of connexin 43 expression by high glucose reduces gap junction activity in microvascular endothelial cells.
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Impairment of retinal vascular homeostasis is associated with the development and progression of diabetic retinopathy involving gap junction intercellular communication (GJIC) activity. The principal gap junction protein of intercellular communication, connexin, was investigated to determine the
Pravastatin normalizes ET-1-induced contraction in the aorta of type 2 diabetic OLETF rats by suppressing the KSR1/ERK complex.
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Endothelin (ET)-1 is a likely candidate for a key role in diabetic vascular complications. In the present study, we hypothesized that treatment with pravastatin (an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase) would normalize the ET-1-induced contraction in aortas isolated from type 2
Osteogenic regulation of vascular calcification.
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Vascular calcification increasingly afflicts our aging and dysmetabolic population, predisposing patients to cardiovascular mortality and lower extremity amputation. Active osteogenic processes are evident in most histoanatomic variants, including elaboration of BMP2-Msx2 signals required for
Association of serum uric acid with bone mineral density and clinical fractures in Chinese type 2 diabetes mellitus patients: A cross-sectional study.
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BACKGROUND
We evaluate the associations of serum uric acid (UA) with bone mineral density (BMD) and prevalence of clinical fractures in type 2 diabetes mellitus (T2DM) patients.
METHODS
1562 T2DM patients undergoing BMD measurement and clinical fractures assessment were enrolled andserum UA
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