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diabetes complications/protease
Veza se sprema u međuspremnik
Stranica 1 iz 57 rezultatima
An Overview on ATP Dependent and Independent Proteases Including an Anterograde to Retrograde Control on Mitochondrial Function; Focus on Diabetes and Diabetic Complications.
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Mitochondria are the central power stations of the cell involved with a myriad of cell signalling pathways that contributes for whole health status of the cell. It is well known fact not only mitochondrial genome encodes for mitochondrial proteins but also there are several mitochondrial specific
Protease inhibitor-induced diabetic complications : incidence, management and prevention.
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Protease inhibitors (PIs) have become a crucial element in the treatment of patients infected with HIV. However, the widespread use of PI therapy has also been associated with a number of metabolic adverse effects, including fat redistribution and hyperglycaemia. The objective of this review is a
Cathepsin S Cleavage of Protease-Activated Receptor-2 on Endothelial Cells Promotes Microvascular Diabetes Complications.
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Endothelial dysfunction is a central pathomechanism in diabetes-associated complications. We hypothesized a pathogenic role in this dysfunction of cathepsin S (Cat-S), a cysteine protease that degrades elastic fibers and activates the protease-activated receptor-2 (PAR2) on endothelial cells. We
Protease profiling of different biofluids in type 1 diabetes mellitus.
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OBJECTIVE
We aimed to disclose the proteolytic events underlying type 1 diabetes and related complication through protease profiling in the bodily fluids serum, urine and saliva.
METHODS
Zymography followed by LC-MS/MS was performed for protease identification and quantitative comparison of
Protease activated receptor 2 in diabetic nephropathy: a double edged sword.
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Diabetic nephropathy is a major microvascular complication of diabetes mellitus, and the leading cause of end stage renal disease worldwide. The pathogenesis of diabetic nephropathy is complex, making the development of novel treatments that stop or reverse the progression of microalbuminuria into
Hyperglycemia potentiates carbonyl stress-induced apoptosis in naïve PC-12 cells: relationship to cellular redox and activator protease factor-1 expression.
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The mechanism(s) of central nervous system complication associated with neurodegenerative disorders such as diabetes is unknown. Previous studies demonstrated that carbonyl stress induced by methylglyoxal (MG) mediates differential apoptosis of rat pheochromocytoma (PC12) cells in the naïve or
In vitro and in vivo prevention of HIV protease inhibitor-induced insulin resistance by a novel small molecule insulin receptor activator.
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Protease inhibitor (PI) therapy for the treatment of patients infected with human immunodeficiency virus is frequently associated with insulin resistance and diabetic complications. These adverse effects of PI treatment result to a large extent from their inhibition of insulin-stimulated glucose
Proteases and protease inhibitors of urinary extracellular vesicles in diabetic nephropathy.
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Diabetic nephropathy (DN) is one of the major complications of diabetes mellitus (DM), leads to chronic kidney disease (CKD), and, ultimately, is the main cause for end-stage kidney disease (ESKD). Beyond urinary albumin, no reliable biomarkers are available for accurate early diagnostics. Urinary
Proteomic analysis of protease resistant proteins in the diabetic rat kidney.
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Glycation induced protein aggregation has been implicated in the development of diabetic complications and neurodegenerative diseases. These aggregates are known to be resistant to proteolytic digestion. Here we report the identification of protease resistant proteins from the streptozotocin induced
Proteases in Plasma and Kidney of db/db Mice as Markers of Diabetes-Induced Nephropathy.
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Db/db mice are overweight, dyslipidemic and develop diabetic complications, relevant for similar complications in human type 2 diabetes. We have used db/db and db/+ control mice to investigate alterations in proteinase expression and activity in circulation and kidneys by SDS-PAGE zymography,
Urinary protein profiles in a rat model for diabetic complications.
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Diabetes mellitus is estimated to affect approximately 24 million people in the United States and more than 150 million people worldwide. There are numerous end organ complications of diabetes, the onset of which can be delayed by early diagnosis and treatment. Although assays for diabetes are well
Fibrosis in diabetes complications: pathogenic mechanisms and circulating and urinary markers.
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Diabetes mellitus is characterized by a lack of insulin causing elevated blood glucose, often with associated insulin resistance. Over time, especially in genetically susceptible individuals, such chronic hyperglycemia can cause tissue injury. One pathological response to tissue injury is the
Advanced glycation end-products and cathepsin cysteine protease in type 2 diabetic patients.
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BACKGROUND
In type 2 diabetes, chronic hyperglycemia induces multi-faceted disturbances and contributes to late diabetic complications. Nonenzymatic glycation, leading to formation of advanced glycation end-products (AGEs), is one of the most important consequences of hyperglycemia. Alterations in
Advanced glycation end products impair protein turnover in LLC-PK1: amelioration by trypsin.
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BACKGROUND
Advanced glycation end products (AGEs) are assumed to play a key role in the pathogenesis of diabetic nephropathy (DN) and other diabetic complications. While AGEs have been shown to exert marked effects on mesangial and endothelial cells as well as on monocytes/macrophages, little is
Carnosine and its possible roles in nutrition and health.
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The dipeptide carnosine has been observed to exert antiaging activity at cellular and whole animal levels. This review discusses the possible mechanisms by which carnosine may exert antiaging action and considers whether the dipeptide could be beneficial to humans. Carnosine's possible biological
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