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diabetic nephropathies/hypoxie

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Up-regulation of hypoxia inducible Factor-1α in patients with diabetic nephropathy.

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To study the role of hypoxia inducible factor-1α (HIF-1α) in patients with diabetic nephropathy (DN).In total, 133 participants were selected to conduct the investigation, parameters such as fasting blood sugar (FBS), blood urea nitrogen (BUN), and urine
The objective of this study was to detect the expression of Angiotensin-II (Ang-II), Hypoxia-inducible factor-1α (HIF-1α) and Endothelin-1 (ET-1) in the kidneys of patients with diabetic nephropathy (DN) and to investigate their relationship with renal interstitial fibrosis (RIF). A total of 47

Mitochondrial Reactive Oxygen Species and Kidney Hypoxia in the Development of Diabetic Nephropathy.

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The underlying mechanisms in the development of diabetic nephropathy are currently unclear and likely consist of a series of dynamic events from the early to late stages of the disease. Diabetic nephropathy is currently without curative treatments and it is acknowledged that even the earliest

Chronic hypoxia exacerbates diabetic glomerulosclerosis through mesangiolysis and podocyte injury in db/db mice

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Background: Chronic hypoxia may play a pivotal role in the development of diabetic nephropathy (DN). However, the precise mechanisms underlying progressive hypoxia-induced glomerular injury remain unclear.

Hypoxia-inducible factor activation in diabetic kidney disease.

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Tissue hypoxia is present in kidneys from diabetic patients and constitutes a central pathway to diabetic kidney disease (DKD). This review summarizes regulation of hypoxia inducible factor (HIF) and interventions towards the same for treatment of DKD. In the hypoxic diabetic kidney, HIF activity

Correlation between polymorphisms of hypoxia-inducible factor-1α Pro582Ser and type 2 diabetic nephropathy.

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We examined the correlation between gene polymorphisms in hypoxia-inducible factor-1α (HIF-1α) Pro582Ser and type 2 diabetic nephropathy (DN). A total of 244 subjects with type 2 diabetes were recruited. The 1285-bp locus polymorphism of HIF-1α exon was detected using polymerase chain

Mechanisms of metabolic memory and renal hypoxia as a therapeutic target in diabetic kidney disease.

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Diabetic kidney disease (DKD) is a worldwide public health problem. The definition of DKD is under discussion. Although the term DKD was originally defined as 'kidney disease specific to diabetes,' DKD frequently means chronic kidney disease with diabetes mellitus and includes not only classical
Today, there is a general lack of prognostic biomarkers for development of renal disease and in particular diabetic nephropathy. Increased glycolytic activity, lactate accumulation and altered mitochondrial oxygen utilization are hallmarks of diabetic kidney disease. Fumarate hydratase activity has
Hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors, also known as HIF stabilizers, increase endogenous erythropoietin production and serve as novel therapeutic agents against anemia in chronic kidney disease. HIF induces the expression of various genes related to energy metabolism as an
BACKGROUND Renal hypoxia plays a role in the development of diabetic nephropathy, and may be mediated by overactivity of the renin-angiotensin-aldosterone system (RAAS). In this study the localization of cellular hypoxia in an experimental model of diabetic nephropathy was assessed, and the effect

Deficiency of hypoxia inducible factor-1α promoted progression of diabetic nephropathy with hypertension.

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The present study was designed to investigate the effect of hypoxia inducible factor-1α (HIF-1α) on diabetic nephropathy (DN) with hypertension. HIF-1α deficient mice (Mx/HIF-1α-/-) were constructed and treated with streptozotocin (STZ) injection for hypertensive DN induction. Normal C57BL/6 mice

Hypoxia-inducible factor-1α is the therapeutic target of the SGLT2 inhibitor for diabetic nephropathy.

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Previous studies have demonstrated intrarenal hypoxia in patients with diabetes. Hypoxia-inducible factor (HIF)-1 plays an important role in hypoxia-induced tubulointerstitial fibrosis. Recent clinical trials have confirmed the renoprotective action of SGLT2 inhibitors in diabetic nephropathy. We

Activation of hypoxia-inducible factors prevents diabetic nephropathy.

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Hyperglycemia results in increased oxygen consumption and decreased oxygen tension in the kidney. We tested the hypothesis that activation of hypoxia-inducible factors (HIFs) protects against diabetes-induced alterations in oxygen metabolism and kidney function. Experimental groups consisted of
BACKGROUND This study aimed to investigate the effects of hirudin on the production of extracellular matrix (ECM) factors by renal tubular epithelial cells in a rat model of diabetic kidney disease (DKD) and HK-2 human renal tubule epithelial cells. MATERIAL AND METHODS Sprague-Dawley rats were
Diabetic kidney disease is the most common cause of end-stage kidney disease and poses a major global health problem. Finding new, safe, and effective strategies to halt this disease has proven to be challenging. In part that is because the underlying mechanisms are complex and not fully understood.
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