Pyridoxamine: The Many Virtues of a Maillard Reaction Inhibitor

Voziyan, Paul A.; Hudson, Billy G.

doi:10.1196/annals.1333.093

Cited by 114 publications

(77 citation statements)

References 60 publications

(103 reference statements)

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“…Our results demonstrate that pyridoxamine does not offer any advantage over aminoguanidine in inhibiting diabetic nephropathy. In addition to inhibition of AGE formation, aminoguanidine is known as an effective free radical scavenger (31), and pyridoxamine has the capacity to scavenge toxic carbonyl products (32). Thus, whereas both aminoguanidine and pyridoxamine inhibit AGE accumulation, additional beneficial properties cannot be excluded.…”

Section: Discussionmentioning

confidence: 99%

Renal Fibrosis and Glomerulosclerosis in a New Mouse Model of Diabetic Nephropathy and Its Regression by Bone Morphogenic Protein-7 and Advanced Glycation End Product Inhibitors

et al. 2007

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Diabetic nephropathy is currently the most common cause of end-stage renal disease (ESRD) in the western world. A mouse model for diabetic nephropathy that encompasses the salient features of this disease in the kidney is not available. Here, we report that CD1 mice, in contrast to inbred C57BL/6 and 129Sv strains, develop ESRD associated with prominent tubulointerstitial nephritis and fibrosis within 3 months and die because of diabetic complications by 6 -7 months after a single injection of streptozotocin. Histopathologic lesions observed in these mice mimic human diabetic nephropathy, including glomerular hypertrophy, diffuse glomerulosclerosis, tubular atrophy, interstitial fibrosis, and decreased renal excretory function. Next, we tested the therapeutic efficacy of bone morphogenic protein-7 (BMP-7) and inhibitors of advanced glycation end products (AGEs), aminoguanidine and pyridoxamine, to inhibit and regress the progression of renal disease in diabetic CD1 mice. We demonstrate that although aminoguanidine, pyridoxamine, and BMP-7 significantly inhibit glomerular lesions, BMP-7 is most effective in the inhibition of tubular inflammation and tubulointerstitial fibrosis in these mice. Collectively, our results report a new mouse model for diabetic nephropathy with prominent interstitial inflammation and fibrosis and the selective inhibition of diabetic kidney disease by AGE inhibitors and BMP-7.

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Section: Discussionmentioning

confidence: 99%

Renal Fibrosis and Glomerulosclerosis in a New Mouse Model of Diabetic Nephropathy and Its Regression by Bone Morphogenic Protein-7 and Advanced Glycation End Product Inhibitors

et al. 2007

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“…Pyridoxamine (PM), one of three natural forms of vitamin B6, was also reported to inhibit the Maillard reaction and PM application in diabetic nephropathy has now progressed to a phase III clinical trials. PM inhibits post-Amadori steps of the Maillard reaction by sequestering catalytic metal ions and blocking the oxidative degradation of Amadori intermediates [190]. Besides vitamin E and PM, α-lipoic acid (ALA) also possesses a strong antioxidant properties [191].…”

Section: Other Anti-glycative Compoudsmentioning

confidence: 99%

Plant-Derived Agents with Anti-Glycation Activity

Odjakova¹,

Popova²,

Sharif³

et al. 2012

Glycosylation

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“…39 The vitamin B6 derivative pyridoxamine (registered as Pyridorin) is a postAmadori inhibitor 192 that traps reactive carbonyl and dicarbonyl compounds derived from Amadori compounds, thereby reducing AGE accumulation. 193,194 Pyridoxamine also scavenges ROS and chelates metal ions (oxidation catalysts). In diabetic rats, pyridoxamine has been shown to decrease AGE and calcification.…”

Section: Antioxidantsmentioning

confidence: 99%

Uremic Toxicity of Advanced Glycation End Products in CKD

Stinghen

Massy

Vlassara

et al. 2016

Journal of the American Society of Nephrology

195

175

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Advanced glycation end products (AGEs), a heterogeneous group of compounds formed by nonenzymatic glycation reactions between reducing sugars and amino acids, lipids, or DNA, are formed not only in the presence of hyperglycemia, but also in diseases associated with high levels of oxidative stress, such as CKD. In chronic renal failure, higher circulating AGE levels result from increased formation and decreased renal clearance. Interactions between AGEs and their receptors, including advanced glycation end product-specific receptor (RAGE), trigger various intracellular events, such as oxidative stress and inflammation, leading to cardiovascular complications. Although patients with CKD have a higher burden of cardiovascular disease, the relationship between AGEs and cardiovascular disease in patients with CKD is not fully characterized. In this paper, we review the various deleterious effects of AGEs in CKD that lead to cardiovascular complications and the role of these AGEs in diabetic nephropathy. We also discuss potential pharmacologic approaches to circumvent these deleterious effects by reducing exogenous and endogenous sources of AGEs, increasing the breakdown of existing AGEs, or inhibiting AGE-induced inflammation. Finally, we speculate on preventive and therapeutic strategies that focus on the AGE-RAGE axis to prevent vascular complications in patients with CKD.

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Pyridoxamine: The Many Virtues of a Maillard Reaction Inhibitor

Cited by 114 publications

References 60 publications

Renal Fibrosis and Glomerulosclerosis in a New Mouse Model of Diabetic Nephropathy and Its Regression by Bone Morphogenic Protein-7 and Advanced Glycation End Product Inhibitors

Renal Fibrosis and Glomerulosclerosis in a New Mouse Model of Diabetic Nephropathy and Its Regression by Bone Morphogenic Protein-7 and Advanced Glycation End Product Inhibitors

Plant-Derived Agents with Anti-Glycation Activity

Uremic Toxicity of Advanced Glycation End Products in CKD

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