diabetic nephropathies/tyrosine

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Evaluation of placental growth factor and soluble Fms-like tyrosine kinase 1 as predictors of all-cause and cardiovascular mortality in patients with Type 1 diabetes with and without diabetic nephropathy.

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OBJECTIVE Placental growth factor is a vascular endothelial growth factor involved in angiogenesis, vascular inflammation and plaque formation. Soluble Fms-like tyrosine kinase 1 is a decoy receptor for placental growth factor, reducing its activity. The aim of this study is to evaluate the

Plasma phenylalanine and tyrosine and their interactions with diabetic nephropathy for risk of diabetic retinopathy in type 2 diabetes

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Objective: Tight control of hyperglycemia reduces risk of diabetic retinopathy (DR), but the residual risk remains high. This study aimed to explore relationships between plasma phenylalanine and tyrosine with DR in type 2 diabetes (T2D)

Spleen tyrosine kinase promotes NLR family pyrin domain containing 3 inflammasome‑mediated IL‑1β secretion via c‑Jun N‑terminal kinase activation and cell apoptosis during diabetic nephropathy.

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Diabetic nephropathy (DN) is a serious complication of diabetes and can cause an increased mortality risk. It was previously reported that NLR family pyrin domain containing 3 (NLRP3) inflammasome is involved in the pathogenesis of diabetes. However, the underlying mechanism is not clearly

Lack of evidence for the 1484insG variant at the 3'-UTR of the protein tyrosine phosphatase 1B (PTP1B) gene as a genetic determinant of diabetic nephropathy development in type 1 diabetic patients.

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Arg tyrosine kinase modulates TGF-β1 production in human renal tubular cells under high-glucose conditions.

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Renal tubular cells are involved in the tubular interstitial fibrosis observed in diabetic nephropathy. It is debated whether epithelial-mesenchymal transition (EMT) affects tubular cells, which under high-glucose conditions overproduce transforming growth factor-β (TGF-β), a fibrogenic cytokine

Flavanomarein inhibits high glucose-stimulated epithelial-mesenchymal transition in HK-2 cells via targeting spleen tyrosine kinase.

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Flavanomarein (FM) is a major natural compound of Coreopsis tinctoria Nutt with protective effects against diabetic nephropathy (DN). In this study, we investigated the effects of FM on epithelial-mesenchymal transition (EMT) in high glucose (HG)-stimulated human proximal tubular epithelial cells

Imatinib attenuates diabetic nephropathy in apolipoprotein E-knockout mice.

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In the diabetic kidney, clinical as well as experimental observations have shown an upregulation of growth factors such as PDGF. These studies, however, were not designed to address whether upregulation of PDGF is merely a manifestation of diabetic renal injury or whether PDGF plays an active role

Novel biphenyl compound, VMNS2e, ameliorates streptozotocin-induced diabetic nephropathy in rats.

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OBJECTIVE To study the effect of a new biphenyl synthetic compound showing interactions with the active site of protein tyrosine phosphatase 1B by docking and molecular dynamics, VMNS2e in streptozotocin-induced diabetic nephropathy in rats with various renal function parameters and renal

Association of the p22phox component of NAD(P)H oxidase with susceptibility to diabetic nephropathy in patients with type 1 diabetes.

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OBJECTIVE Increased production of reactive oxygen species (ROS) in diabetes is thought to play a major role in the pathogenesis of diabetic microvascular complications such as nephropathy and retinopathy. The NAD(P)H oxidase complex is an important source of ROS in the vasculature. The p22 subunit

Identification of key genes for diabetic kidney disease using biological informatics methods.

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Diabetic kidney disease (DKD) is a common complication of diabetes, which is characterized by albuminuria, impaired glomerular filtration rate or a combination of the two. The aim of the present study was to identify the potential key genes involved in DKD progression and to subsequently investigate

Increased carbonyl modification by lipids and carbohydrates in diabetic nephropathy.

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BACKGROUND In diabetic nephropathy (DN), possible mediators of untoward effects of hyperglycemia include the advanced glycation end products (AGEs). Indeed, an AGE, carboxymethyllysine (CML), accumulates in expanded mesangial matrix and nodular lesions. An advanced lipoxidation end product (ALE),

Insulin receptor substrate-2 is expressed in kidney epithelium and up-regulated in diabetic nephropathy.

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Diabetic nephropathy (DN) is a progressive fibrotic condition that may lead to end-stage renal disease and kidney failure. Transforming growth factor-β1 and bone morphogenetic protein-7 (BMP7) have been shown to induce DN-like changes in the kidney and protect the kidney from such changes,

HDL causes mesangial cell mitogenesis through a tyrosine kinase-dependent receptor mechanism.

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Hypercholesterolemia and mesangial cell proliferation have been proposed to play a role in the progression of glomerulosclerosis in diabetic nephropathy and other renal diseases. Although LDL is mitogenic for and cytotoxic to mesangial cells, the effect of HDL on these cells is unknown. HDL

Angiotensin-(1-7) activates a tyrosine phosphatase and inhibits glucose-induced signalling in proximal tubular cells.

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BACKGROUND In the diabetic kidney, stimulation of mitogen-activated protein kinases (MAPKs) leads to extracellular matrix protein synthesis. In the proximal tubule, angiotensin-(1-7) [Ang-(1-7)] blocks activation of MAPKs by angiotensin II. We studied the effect of Ang-(1-7) on signalling responses

QiDiTangShen Granules Reduced Diabetic Kidney Injury by Regulating the Phosphorylation Balance of the Tyrosine and Serine Residues of Insulin Receptor Substrate 1.

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UNASSIGNED Diabetic nephropathy (DN) is a microvascular complication induced by diabetes mellitus (DM), which can affect life quality and long-term prognosis of patients with DM. Angiotensin-converting-enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB) are currently recommended for

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