Advanced glycation end products and vascular structure and function

  title={Advanced glycation end products and vascular structure and function},
  author={Georgia Soldatos and Mark Emmanuel Cooper},
  journal={Current Hypertension Reports},
Diabetes mellitus has now reached epidemic proportions in the Western world. The associated microvascular and macrovascular complications are a result of severe metabolic derangement, which leads to chronic tissue injury. Although there are a number of proposed pathophysiologic mechanisms for the vascular complications associated with diabetes, this review focuses predominantly on the role of advanced glycation end products (AGEs) in the pathogenesis of diabetes-associated atherosclerosis. The… 

Advanced Glycation End Products and Diabetic Cardiovascular Disease

The present review summarizes the relevant evidence supporting the role of advanced glycation in promoting atherosclerosis and the epidemiologic studies demonstrating an association between AGEs and diabetic cardiovascular disease.

Advanced Glycation End Products Accumulate in Vascular Smooth Muscle and Modify Vascular but Not Ventricular Properties in Elderly Hypertensive Canines

In elderly hypertensive canines, AGE accumulation and AGE cross-link breaker effects were confined to the vasculature without evidence of myocardial accumulation or effects, which suggests that the striking vascular effects may be mediated by mechanisms other than collagen cross-linking.

Advanced glycation end-products in senile diabetic and non-diabetic patients with cardiovascular complications

The AGEs distribution in the senile groups corroborates the hypothesis that the advanced glycation process might play a role in the development of cardiovascular complications, which are more severe in diabetic patients compared with non-diabetic patients with cardiovascular complications.

Advanced Glycation End Products Accumulate in Vascular Smooth Muscle and Modify Vascular but Not Ventricular Properties in Elderly Hypertensive Canines Heart Failure

In elderly hypertensive canines, AGE accumulation and AGE cross-link breaker effects were confined to the vasculature without evidence of myocardial accumulation or effects, suggesting that this therapeutic strategy may favorably modify arterial properties but also that such therapies may be associated with aortic dilatation, at least in the setting of persistent hypertension.

Matrix Biology of Abdominal Aortic Aneurysms in Diabetes: Mechanisms Underlying the Negative Association

The aim of the present minireview is to compare the changes in matrix biology seen in diabetes and AAA and to explore molecular mechanisms that may explain the negative association and identify possible therapeutic implications.

Association between Advanced Glycation End Products, Soluble RAGE Receptor, and Endothelium Dysfunction, Evaluated by Circulating Endothelial Cells and Endothelial Progenitor Cells in Patients with Mild and Resistant Hypertension

It may be concluded that the level of AGEs may be an independent predictor of the condition and function of the endothelium and sRAGE may be classified as a potential biomarker of inflammation and endothelial dysfunction.

Possible Involvement of Advanced Glycation End Products in Periodontal Diseases

The present study highlights the need for further investigation on the presence of AGEs in the periodontal ligament as a means for the comprehension of the pathogenic mechanisms underlyingperiodontal diseases in order to develop prevention and treatment modalities for this dysfunction.

Nitrate and Nitrite in Aging and Age-Related Disease

Collectively, current evidence suggests that nitrate and nitrite supplementation represent promising therapeutic strategies for enhancing physiological function with aging and reducing the risk of age-associated disability and risk of chronic diseases.

Increased glycated albumin and decreased esRAGE concentrations are associated with in-stent restenosis in Chinese diabetic patients.

  • Lin LuLi Jin Pu W. Shen
  • Medicine
    Clinica chimica acta; international journal of clinical chemistry
  • 2008

Oxidative stress in myocardial infarction: Advanced glycation end-products causes oxidative stress in older myocardial infarction patients

It was revealed that AGE was positively associated with markers of oxidative stress in the older groups, and malondialdehyde and serum AGE were found to be significantly higher in older diabetic and non-diabetic patients with and without myocardial infarction as compared with young control subjects.



Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts

Findings indicate interaction between the advanced glycation endproducts and their receptor is involved in the development of accelerated atherosclerosis in diabetes, and identify this receptor as a new therapeutic target in diabetic macrovascular disease.

Advanced glycation end product interventions reduce diabetes-accelerated atherosclerosis.

AlT-711 and AG demonstrated the ability to reduce vascular AGE accumulation in addition to attenuating atherosclerosis in these diabetic mice.

Breakers of advanced glycation end products restore large artery properties in experimental diabetes.

Treatment of rats with streptozotocin-induced diabetes with the AGE-breaker ALT-711 for 1-3 weeks reversed the diabetes-induced increase of large artery stiffness as measured by systemic arterial compliance, aortic impedance, and carotid artery compliance and distensibility.

Lipid and lipoprotein modification by advanced glycosylation end‐products: role in atherosclerosis

  • R. Bucala
  • Medicine, Biology
    Experimental physiology
  • 1997
A dyslipidaemia characterized by increased levels of LDL, very low-density lipoprotein (VLDL) and intermediate-density cholesterol (IDL) occurs commonly in diabetes and significantly increases the likelihood that patients will suffer from the atherosclerotic complications of heart attack and stroke.

Expression of receptors for advanced glycation end products in peripheral occlusive vascular disease.

The data suggest that RAGE is likely to have ligands other than AGEs, and that multiple factors in addition to A GEs impact on its expression, suggesting that RAGES may contribute to the pathogenesis of a range of vascular disorders.

Advanced glycation end products in nondiabetic patients with coronary artery disease.

This pilot study indicates the relation between AGEs and the severity of CAD in nondiabetic patients and the measurement of serum AGE concentrations may be predictive of vascular damage.

Advanced glycosylation end products in patients with diabetic nephropathy.

AGEs accumulate at a faster-than-normal rate in arteries and the circulation of patients with diabetes; the increase in circulating AGE peptides parallels the severity of renal functional impairment in diabetic nephropathy.

Advanced protein glycosylation in diabetes and aging.

  • M. Brownlee
  • Biology, Medicine
    Annual review of medicine
  • 1995
Pharmacologic inhibition of AGE formation in long-term diabetic animals prevents diabetic retinopathy, nephropathy, neuropathy, and arterial abnormalities in animal models and in humans is currently in progress.

Plasma Levels of Soluble Receptor for Advanced Glycation End Products and Coronary Artery Disease in Nondiabetic Men

The findings indicate that low levels of sRAGE in plasma are independently associated with the presence of CAD in nondiabetic men and suggest that sRAge is one of the clinically important molecules associated with atherosclerosis.

Aminoguanidine prevents diabetes-induced arterial wall protein cross-linking.

The identification of aminoguanidine as an inhibitor of advanced nonenzymatic glycosylation product formation makes possible precise experimental definition of the pathogenetic significance of this process and suggests a potential clinical role for aminogsuanidine in the future treatment of chronic diabetic complications.