Renal accumulation and clearance of advanced glycation end-products in type 2 diabetic nephropathy: effect of angiotensin-converting enzyme and vasopeptidase inhibition

Wihler, Cornelia; Schäfer, Stefan; Schmid, K.; Deemer, Elizabeth K.; Münch, Gerald; Bleich, Markus; Büsch, Andreas; Dingermann, Theo; Somoza, Veronika; Baynes, John W.; Huber, J.

doi:10.1007/s00125-005-1837-9

Cited by 42 publications

(28 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These agents include aminoguanidine, AVE7688, pyridoxamine, carnosine, benfotiamine, OPB-9195, LR-90, and the so-called cross-link breakers such as ALT-946 and thiazolium salts (e.g., N-phenacylthiazolium bromide and alagebrium chloride) [116,117,[124][125][126][127][128]. In addition, it has been demonstrated that a number of established therapies have the ability to reduce the accumulation of AGEs/ALEs in diabetes, including angiotensin converting enzyme inhibitors, angiotensin receptor antagonists, metformin, peroxisome proliferators receptor agonists, metal chelators and some antioxidants [116,117,119,[124][125][126][127].…”

Section: Is Protein Carbonylation An Early Event Of Cellular Dysfunctmentioning

confidence: 99%

Protein carbonylation, cellular dysfunction, and disease progression

Dalle‐Donne

Aldini

Colombo

et al. 2006

Journal of Cellular and Molecular Medicine

728

545

View full text Add to dashboard Cite

Carbonylation of proteins is an irreversible oxidative damage, often leading to a loss of protein function, which is considered a widespread indicator of severe oxidative damage and disease-derived protein dysfunction. Whereas moderately carbonylated proteins are degraded by the proteasomal system, heavily carbonylated proteins tend to form high-molecular-weight aggregates that are resistant to degradation and accumulate as damaged or unfolded proteins. Such aggregates of carbonylated proteins can inhibit proteasome activity. A large number of neurodegenerative diseases are directly associated with the accumulation of proteolysis-resistant aggregates of carbonylated proteins in tissues. Identification of specific carbonylated protein(s) functionally impaired and development of selective carbonyl blockers should lead to the definitive assessment of the causative, correlative or consequential role of protein carbonylation in disease onset and/or progression, possibly providing new therapeutic aproaches.

show abstract

Section: Is Protein Carbonylation An Early Event Of Cellular Dysfunctmentioning

confidence: 99%

Protein carbonylation, cellular dysfunction, and disease progression

Dalle‐Donne

Aldini

Colombo

et al. 2006

Journal of Cellular and Molecular Medicine

728

545

View full text Add to dashboard Cite

show abstract

“…The binding with tristetraprolin increases its molecular weight and prevents its filtration and catabolism in the kidney (Vahlquist et al, 1973;Goodman, 1980;Kiernan et al, 2002;Wihler et al, 2005;Yang et al, 2005). After releasing ROH into the target cells, the remaining apo-RBP4 (unbound ROH) is quickly filtered through the glomeruli and reabsorbed into the proximal tubules via the megalin-cubilin receptor complex, and then catabolized (Peterson and Berggard, 1971;Mogielnicki et al, 1971;Raila et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Decreased retinol-binding protein 4 in the sera of patients with end-stage renal disease after kidney transplantation

Zhang¹,

Zhou²,

Zhang³

et al. 2014

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Retinol-binding protein 4 (RBP4) is a novel adipokine that has been associated with insulin resistance and type 2 diabetes. Patients with end-stage renal disease (ESRD) have very high serum RBP4 levels. However, whether successful kidney transplantation alleviates these elevated serum RBP4 levels is unclear. The serum RBP4 levels of 24 ESRD patients were determined before transplantation and at 1 day, 1 week, and 1 month after kidney transplantation. The control group included 22 healthy subjects. Serum RBP4 concentrations were measured using a commercial kit via the immunologic turbidimetric method, and were related to biomarkers for renal and liver function. The serum RBP4 level of ESRD patients before kidney transplantation (160.8 ± 29.1 mg/L) was Level of RBP4 in patients after kidney transplantation approximately 7-fold higher than that of normal controls (22.6 ± 11.0 mg/L; P = 0.000). The serum RBP4 level before transplantation was significantly higher than that at 1 day (65.3 ± 28.4 mg/L), 1 week (48.3 ± 22.9 mg/L), and 1 month after transplantation (53.1 ± 25.5 mg/L; P = 0.000). However, these values were still higher than those of controls (P = 0.000). Univariate regression analysis showed that the percent changes in serum RBP4 concentration before and after kidney transplantation were positively correlated with serum creatinine, blood urea nitrogen, phosphate, and pre-albumin concentrations and negatively correlated with the estimated glomerular filtration rate. The serum RBP4 concentration of patients with ESRD decreased significantly after kidney transplantation; therefore, we found that serum RBP4 concentration was related to renal function.

show abstract

“…In this regard, vascular conductance in the femoral artery of streptozotocin-induced diabetic rats was improved by a vasopeptidase inhibitor (21). Vasopeptidase inhibitors are neuroprotective and prevent nephropathy in ZDF rats; they have also been reported to decrease matrix metalloproteinases and advanced glycosylation end product accumulation/formation in type 2 diabetes and to improve wound healing (22)(23)(24)(25)(26)(27)(28). Therefore, there is great potential for treatment of diabetic neuropathy with vasopeptidase inhibitors; however, no information is available.…”

mentioning

confidence: 99%

Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

et al. 2007

View full text Add to dashboard Cite

In epineurial arterioles, acetylcholine-mediated vascular relaxation is mediated by nitric oxide and endotheliumderived hyperpolarizing factor (EDHF), and both mechanisms are impaired by diabetes. The mediator responsible for the effect of EDHF is unknown. In epineurial arterioles, C-type natriuretic peptide (CNP) has properties consistent with EDHF-like activity. Epineurial arterioles express CNP, and exogenous CNP causes a concentration-dependent vascular relaxation. In streptozotocin-induced diabetic rats, CNP-mediated vascular relaxation in epineurial arterioles is decreased. Since CNP may be a regulator of vascular function, a vasopeptidase inhibitor may be an effective treatment for diabetes-induced vascular and neural disease. Vasopeptidase inhibitors inhibit ACE activity and neutral endopeptidase, which degrades natriuretic peptides. Streptozotocin-induced diabetic rats were treated with AVE7688 (450 mg/kg in the diet), a vasopeptidase inhibitor, for 8 -10 weeks after 4 weeks of untreated diabetes. Treatment of diabetic rats corrected the diabetesinduced decrease in endoneurial blood flow, significantly improved motor and sensory nerve conduction velocity, prevented the development of hypoalgesia in the hind paw, and reduced superoxide and nitrotyrosine levels in epineurial arterioles. The diabetes-induced decrease in acetylcholine-mediated vascular relaxation by epineurial arterioles was significantly improved with treatment. These studies suggest that vasopeptidase inhibitors may be an effective approach for the treatment of diabetic vascular and neural dysfunction. Diabetes 56:355-362, 2007 S tudies performed in our laboratory with streptozotocin-induced diabetic rats have provided evidence that the generation of oxidative stress through the production of superoxide and peroxynitrite impairs vascular function of epineurial arterioles of the sciatic nerve, and this precedes slowing of motor nerve conduction velocity (MNCV) (1-3). These studies imply that hyperglycemia-induced oxidative stress may be responsible for diabetes-induced vascular and neural dysfunction that occurs during diabetic neuropathy.We have recently reported that the ACE inhibitor Enalapril was an effective treatment for vascular and neural disease in streptozotocin-induced diabetic rats (4). These results and our studies with C-type natriuretic peptide (CNP), demonstrating its vascular relaxation properties in epineurial arterioles, provide rationale to test the effect of vasopeptidase inhibitors on diabetic neuropathy.It has been reported in mesenteric resistance arteries that release of CNP accounts for the biological activity of endothelium-derived hyperpolarizing factor (EDHF) (5,6). CNP was found to be released from endothelial cells of the perfused rat mesenteric bed in response to endotheliumdependent vasodilators such as acetylcholine (5,6). CNP induced hyperpolarization and relaxation of mesenteric artery vascular smooth muscle through activation of natriuretic peptide receptor subtype B and the same potassium channels that...

show abstract

Renal accumulation and clearance of advanced glycation end-products in type 2 diabetic nephropathy: effect of angiotensin-converting enzyme and vasopeptidase inhibition

Cited by 42 publications

References 45 publications

Protein carbonylation, cellular dysfunction, and disease progression

Protein carbonylation, cellular dysfunction, and disease progression

Decreased retinol-binding protein 4 in the sera of patients with end-stage renal disease after kidney transplantation

Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

Contact Info

Product

Resources

About