diabetic nephropathies/prolinas

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Metabolic reprogramming by N-acetyl-seryl-aspartyl-lysyl-proline protects against diabetic kidney disease.

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Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) are first-line conventional drugs that are believed to reduce the progression of end-stage renal disease in diabetic patients. However, differences in the effects of ACEi and ARB are well not

N-acetyl-seryl-aspartyl-lysyl-proline prevents renal insufficiency and mesangial matrix expansion in diabetic db/db mice.

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We have previously reported that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is a tetrapeptide hydrolyzed by ACE, inhibits the transforming growth factor-beta (TGF-beta)-induced expression of extracellular matrix proteins via inhibition of the Smad signaling in human mesangial cells. To

Metabolomics window into the role of acute kidney injury after coronary artery bypass grafting in diabetic nephropathy progression

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Introduction: Metabolomics has emerged as a valuable tool to discover novel biomarkers and study the pathophysiology of diabetic nephropathy (DN). However, the effect of postoperative acute kidney injury (AKI) on diabetes mellitus (DM) to chronic DN progression has

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

Leucine 7 to proline 7 polymorphism in the preproneuropeptide Y is associated with proteinuria, coronary heart disease, and glycemic control in type 1 diabetic patients.

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OBJECTIVE Neuropeptide Y is a potent vasoconstrictor thought to enhance the development of atherosclerosis. The leucine 7 to proline 7 (Leu7Pro) polymorphism, located in the signal peptide part of the human preproneuropeptide Y, has been associated with serum lipid levels, intima-media thickness of

Peroxisome proliferator activated receptor γ2 gene Pro12Ala gene polymorphism in type 2 diabetes and its relationship with diabetic nephropathy.

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BACKGROUND Despite intensive research, a genetic background of type 2 diabetes is still unknown as are causes of differences in the clinical course of the disease. This supports the hypothesis for factors of genetic susceptibility (or protection) to diabetic nephropathy. This study aimed to examine

Meprin beta metalloprotease gene polymorphisms associated with diabetic nephropathy in the Pima Indians.

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There is evidence that susceptibility to diabetic nephropathy has a significant genetic component. This investigation tested the hypothesis that variations in the structural or regulatory regions of the MEP1B gene are related to susceptibility to diabetic nephropathy in the Pima Indian population.

Renal antifibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats.

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OBJECTIVE Diabetic nephropathy is the main cause of end-stage renal disease. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a physiological tetrapeptide hydrolyzed by the angiotensin-converting enzyme (ACE), has antifibrotic effects in the cardiovascular system and in the kidney in experimental

Identification of hub genes in diabetic kidney disease via multiple-microarray analysis

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Background: Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease; however, the underlying molecular mechanisms remain unclear. Recently, bioinformatics analysis has provided a comprehensive insight toward the

Thiazolidinediones ameliorate diabetic nephropathy via cell cycle-dependent mechanisms.

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Thiazolidinediones are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, widely used as insulin sensitizer in type 2 diabetic patients and implicated in apoptosis, cell proliferation, and cell cycle regulation. Here, the effect of thiazolidinediones on G1-phase cell cycle arrest,

Oral Administration of N-Acetyl-seryl-aspartyl-lysyl-proline Ameliorates Kidney Disease in Both Type 1 and Type 2 Diabetic Mice via a Therapeutic Regimen.

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Kidney fibrosis is the final common pathway of progressive kidney diseases including diabetic nephropathy. Here, we report that the endogenous antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), the substrate of angiotensin-converting enzyme (ACE), is an orally available peptide

The Absence of the ACE N-Domain Decreases Renal Inflammation and Facilitates Sodium Excretion during Diabetic Kidney Disease.

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BACKGROUND Recent evidence emphasizes the critical role of inflammation in the development of diabetic nephropathy. Angiotensin-converting enzyme (ACE) plays an active role in regulating the renal inflammatory response associated with diabetes. Studies have also shown that ACE has roles in

N-acetyl-seryl-aspartyl-lysyl-proline: a valuable endogenous anti-fibrotic peptide for combating kidney fibrosis in diabetes.

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Fibroproliferative diseases are responsible for 45% of deaths in the developed world. Curing organ fibrosis is essential for fibroproliferative diseases. Diabetic nephropathy is a common fibroproliferative disease of the kidney and is associated with multiorgan dysfunction. However, therapy to

Expression, localization, and function of the thioredoxin system in diabetic nephropathy.

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Excessive reactive oxygen species play a key role in the pathogenesis of diabetic nephropathy, but to what extent these result from increased generation, impaired antioxidant systems, or both is incompletely understood. Here, we report the expression, localization, and activity of the antioxidant

Berberine reduces fibronectin and collagen accumulation in rat glomerular mesangial cells cultured under high glucose condition.

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Diabetic nephropathy, one of the microvascular complications of diabetes mellitus, is a leading cause of end-stage renal disease. Berberine is one of the main constituents of Coptidis Rhizoma and Cortex Phellodendri. In this study, we investigated the effects of berberine on fibronectin and collagen

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