H Vlassara

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. ncbi request reprint Diet-derived advanced glycation end products are major contributors to the body's AGE pool and induce inflammation in healthy subjects
    Jaime Uribarri
    Division of Nephrology, Deparment of Medicine, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Ann N Y Acad Sci 1043:461-6. 2005
  2. pmc Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan
    Weijing Cai
    Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Am J Pathol 173:327-36. 2008
  3. pmc Managing chronic inflammation in the aging diabetic patient with CKD by diet or sevelamer carbonate: a modern paradigm shift
    H Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics and Palliative Care, Mount Sinai School of Medicine, 1 Gustave Levy Place, NY 10029, USA
    J Gerontol A Biol Sci Med Sci 67:1410-6. 2012
  4. ncbi request reprint The role of advanced glycation end products in the development of atherosclerosis
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, The Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029, USA
    Curr Diab Rep 4:31-6. 2004
  5. pmc Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Proc Natl Acad Sci U S A 99:15596-601. 2002
  6. ncbi request reprint Glycoxidation and diabetic complications: modern lessons and a warning?
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA
    Rev Endocr Metab Disord 5:181-8. 2004
  7. ncbi request reprint Glycotoxins in the diet promote diabetes and diabetic complications
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
    Curr Diab Rep 7:235-41. 2007
  8. ncbi request reprint Glycoxidation: the menace of diabetes and aging
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Box 1640, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA
    Mt Sinai J Med 70:232-41. 2003
  9. doi request reprint Advanced glycation end product homeostasis: exogenous oxidants and innate defenses
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann N Y Acad Sci 1126:46-52. 2008
  10. pmc Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Clin Endocrinol Metab 94:4483-91. 2009

Research Grants

  1. AGING AND VASCULAR DISEASE: ROLE OF GLYCATION
    Helen Vlassara; Fiscal Year: 2007
  2. Effects of Glycoxidative Stress on Human Aging
    Helen Vlassara; Fiscal Year: 2010
  3. Vascular Response and Glycoxidant Homeostasis
    Helen Vlassara; Fiscal Year: 2007
  4. Effects of Glycoxidative Stress on Human Aging
    Helen Vlassara; Fiscal Year: 2007
  5. Vascular Response and Glycoxidant Homeostasis
    Helen Vlassara; Fiscal Year: 2009
  6. AGING AND VASCULAR DISEASE--ROLE OF GLYCATION
    Helen Vlassara; Fiscal Year: 2001
  7. AGE-RECEPTORS AND KIDNEY DISEASE
    Helen Vlassara; Fiscal Year: 2003

Collaborators

Detail Information

Publications57

  1. ncbi request reprint Diet-derived advanced glycation end products are major contributors to the body's AGE pool and induce inflammation in healthy subjects
    Jaime Uribarri
    Division of Nephrology, Deparment of Medicine, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Ann N Y Acad Sci 1043:461-6. 2005
    ..Together with previous evidence from diabetics and renal failure patients, these data suggest that dietary AGEs may play an important role in the causation of chronic diseases associated with underlying inflammation...
  2. pmc Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan
    Weijing Cai
    Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Am J Pathol 173:327-36. 2008
    ..Therefore, the beneficial effects of a CR diet may be partly related to reduced oxidant intake, a principal determinant of oxidant status in aging mice, rather than decreased energy intake...
  3. pmc Managing chronic inflammation in the aging diabetic patient with CKD by diet or sevelamer carbonate: a modern paradigm shift
    H Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics and Palliative Care, Mount Sinai School of Medicine, 1 Gustave Levy Place, NY 10029, USA
    J Gerontol A Biol Sci Med Sci 67:1410-6. 2012
    ..If larger and longer studies confirm the hypothesis that one or both of these interventions reduce progression of CKD, it could represent a new paradigm in the management of complications in the type 2 diabetes patient with CKD...
  4. ncbi request reprint The role of advanced glycation end products in the development of atherosclerosis
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, The Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029, USA
    Curr Diab Rep 4:31-6. 2004
    ..An increased understanding of the mechanisms of formation and interaction of AGEs has allowed the development of several potential anti-AGE approaches...
  5. pmc Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Proc Natl Acad Sci U S A 99:15596-601. 2002
    ..05). Thus in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury. Restriction of dietary AGEs suppresses these effects...
  6. ncbi request reprint Glycoxidation and diabetic complications: modern lessons and a warning?
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA
    Rev Endocr Metab Disord 5:181-8. 2004
  7. ncbi request reprint Glycotoxins in the diet promote diabetes and diabetic complications
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
    Curr Diab Rep 7:235-41. 2007
    ..This beneficial outcome requires only a 50% decrease in dietary AGEs, making this necessary intervention practical and inexpensive...
  8. ncbi request reprint Glycoxidation: the menace of diabetes and aging
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Box 1640, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA
    Mt Sinai J Med 70:232-41. 2003
    ..AGE toxicity may be averted by promising dietary and pharmacological strategies which are currently being investigated...
  9. doi request reprint Advanced glycation end product homeostasis: exogenous oxidants and innate defenses
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann N Y Acad Sci 1126:46-52. 2008
    ..In both humans and mice, there was an inverse correlation between the AGER1 to RAGE ratio and the levels of OS...
  10. pmc Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1
    Helen Vlassara
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Clin Endocrinol Metab 94:4483-91. 2009
    ..Whereas AGE receptor-1 (AGER1) reduces OS/infl in animals, this has not been assessed in normal humans...
  11. ncbi request reprint Diabetes and advanced glycation endproducts
    H Vlassara
    Department of Geriatrics, Mount Sinai School of Medicine, NY 10029, USA
    J Intern Med 251:87-101. 2002
    ..The final disposal of AGE depends on renal clearance. Promising pharmacologic strategies to prevent AGE formation, reduce AGE toxicity, and/or inactivate AGE are under investigation...
  12. doi request reprint Identifying advanced glycation end products as a major source of oxidants in aging: implications for the management and/or prevention of reduced renal function in elderly persons
    Helen Vlassara
    Division of Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Semin Nephrol 29:594-603. 2009
    ..These data suggest that the changes in renal function in normal aging may be subject to control and this subject deserves renewed attention...
  13. ncbi request reprint The AGE-receptor in the pathogenesis of diabetic complications
    H Vlassara
    Mount Sinai School of Medicine, New York, NY 10029, USA
    Diabetes Metab Res Rev 17:436-43. 2001
    ..Various AGE-binding peptides or soluble receptors have emerged as potential sequestering agents for toxic AGEs as potential therapies for diabetic complications...
  14. ncbi request reprint Advanced glycation in health and disease: role of the modern environment
    Helen Vlassara
    Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
    Ann N Y Acad Sci 1043:452-60. 2005
    ....
  15. ncbi request reprint Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake
    Oana Sandu
    The Brookdale Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029, USA
    Diabetes 54:2314-9. 2005
    ..05). These results demonstrate that the development of insulin resistance and type 2 diabetes during prolonged high-fat feeding are linked to the excess AGEs/advanced lipoxidation end products inherent in fatty diets...
  16. ncbi request reprint Advanced glycoxidation end products in commonly consumed foods
    Teresia Goldberg
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Am Diet Assoc 104:1287-91. 2004
    ..The objective of this article was to determine the AGE content of commonly consumed foods and to evaluate the effects of various methods of food preparation on AGE production...
  17. pmc Reduced oxidant stress and extended lifespan in mice exposed to a low glycotoxin diet: association with increased AGER1 expression
    Weijing Cai
    Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
    Am J Pathol 170:1893-902. 2007
    ..A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice...
  18. pmc Circulating glycotoxins and dietary advanced glycation endproducts: two links to inflammatory response, oxidative stress, and aging
    Jaime Uribarri
    Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Gerontol A Biol Sci Med Sci 62:427-33. 2007
    ..AGEs are readily derived from heat-treated foods. We propose that the excess consumption of certain AGEs via the diet enhances OS and inflammatory responses in healthy adults, especially in elderly persons...
  19. ncbi request reprint Glycoxidation and inflammation in renal failure patients
    Melpomeni Peppa
    Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029, USA
    Am J Kidney Dis 43:690-5. 2004
    ..Advanced glycoxidation end products (AGEs) are among the factors implicated in the inflammatory state of chronic renal failure...
  20. pmc Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidative stress, and post-injury intimal hyperplasia
    Massimo Torreggiani
    Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Am J Pathol 175:1722-32. 2009
    ....
  21. ncbi request reprint High levels of dietary advanced glycation end products transform low-density lipoprotein into a potent redox-sensitive mitogen-activated protein kinase stimulant in diabetic patients
    Weijing Cai
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Circulation 110:285-91. 2004
    ..It remains unclear, however, whether exogenous (diet-derived) AGEs influence glycoxidation and endothelial cell toxicity of diabetic LDL...
  22. pmc Endothelial dysfunction in patients with chronic kidney disease results from advanced glycation end products (AGE)-mediated inhibition of endothelial nitric oxide synthase through RAGE activation
    Ellena Linden
    Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Clin J Am Soc Nephrol 3:691-8. 2008
    ....
  23. ncbi request reprint Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, New York, NY 10029, USA
    Diabetes 52:1441-8. 2003
    ..005). Therefore, high AGE intake may provide excess antigenic stimulus for T-cell-mediated diabetes or direct beta-cell injury in NOD mice; both processes are ameliorated by maternal or neonatal exposure to L-AGE nutrition...
  24. ncbi request reprint Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice
    Reigh Yi Lin
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, One Gustave L Levy Place, New York, NY 10029, USA
    Atherosclerosis 168:213-20. 2003
    ..The marked anti-atherogenic effects of an AGE-restricted diet in this model may provide the basis for relevant clinical studies...
  25. pmc Presence of diabetic complications in type 1 diabetic patients correlates with low expression of mononuclear cell AGE-receptor-1 and elevated serum AGE
    C J He
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
    Mol Med 7:159-68. 2001
    ....
  26. pmc AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-delta: implications for vascular disease
    Weijing Cai
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
    Am J Physiol Cell Physiol 298:C624-34. 2010
    ..In conclusion, circulating AGEs induce NADPH-dependent ROS generation in vascular aging in both in vitro and in vivo models. Furthermore, AGER1 provides protection against AGE-induced ROS generation via NADPH...
  27. ncbi request reprint AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation
    Weijing Cai
    Division of Diabetes and Aging Research, The Brookdale Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10019, USA
    Am J Physiol Cell Physiol 294:C145-52. 2008
    ..This represents a key mechanism by which AGER1 maintains cellular resistance against OS. Thus the decrease of AGER1 noted in aging and diabetes may further enhance OS and reduce innate antioxidant defenses...
  28. ncbi request reprint Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients
    Jaime Uribarri
    Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Am Soc Nephrol 14:728-31. 2003
    ..Moreover, dietary restriction of AGE is an effective and feasible method to reduce excess toxic AGE and possibly cardiovascular associated mortality...
  29. ncbi request reprint Single oral challenge by advanced glycation end products acutely impairs endothelial function in diabetic and nondiabetic subjects
    Jaime Uribarri
    Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, One Gustave Levy Pl, New York, NY 10029, USA
    Diabetes Care 30:2579-82. 2007
    ..The current study was designed to test the acute effects of dietary advanced glycation end products (AGEs) on endothelial function of diabetic and nondiabetic subjects...
  30. pmc Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction
    Weijing Cai
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Mol Med 8:337-46. 2002
    ..AGE-rich foods could exacerbate diabetic injury, at least by raising the endogenous AGE...
  31. ncbi request reprint Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse
    Susanna M Hofmann
    Brookdale Department of Genetics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029 6574, USA
    Diabetes 51:2082-9. 2002
    ..02). These results demonstrate that reduced AGE intake leads to lower levels of circulating AGE and to improved insulin sensitivity in db/db mice...
  32. ncbi request reprint Lowering of dietary advanced glycation endproducts (AGE) reduces neointimal formation after arterial injury in genetically hypercholesterolemic mice
    Reigh Yi Lin
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, Box 1640, One Gustave L Levy Place, New York, NY 10029 6574, USA
    Atherosclerosis 163:303-11. 2002
    ....
  33. pmc Advanced glycation end products inhibit glucose-stimulated insulin secretion through nitric oxide-dependent inhibition of cytochrome c oxidase and adenosine triphosphate synthesis
    Zhengshan Zhao
    Department of Geriatrics and Adult Development, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
    Endocrinology 150:2569-76. 2009
    ..We conclude that AGEs inhibit cytochrome c oxidase and ATP production, leading to the impairment of glucose-stimulated insulin secretion through iNOS-dependent nitric oxide production...
  34. pmc Induction of diabetes in aged C57B6 mice results in severe nephropathy: an association with oxidative stress, endoplasmic reticulum stress, and inflammation
    Jin Wu
    Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    Am J Pathol 176:2163-76. 2010
    ..The expression of tumor-necrosis factor-alpha in 22-month-old diabetic kidneys may play a role in inflammation, ER stress, and apoptosis. Thus, diabetes may accelerate the underlying kidney aging process present in old mice...
  35. pmc Advanced glycation end product (AGE) receptor 1 suppresses cell oxidant stress and activation signaling via EGF receptor
    Weijing Cai
    Division of Experimental Diabetes and Aging, Brookdale Department of Geriatrics, and Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    Proc Natl Acad Sci U S A 103:13801-6. 2006
    ..AGER1 could serve as a model for developing therapeutic targets against vascular and kidney disorders related to diabetes and aging...
  36. ncbi request reprint Adverse effects of dietary glycotoxins on wound healing in genetically diabetic mice
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, New York 10029, USA
    Diabetes 52:2805-13. 2003
    ..Thus, increased diet-derived AGE intake may be a significant retardant of wound closure in diabetic mice; dietary AGE restriction may improve impaired diabetic wound healing...
  37. ncbi request reprint Advanced glycoxidation. A new risk factor for cardiovascular disease?
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Cardiovasc Toxicol 2:275-87. 2002
    ..Prospective outcome and controlled studies are needed to further support this relationship...
  38. ncbi request reprint Dietary glycotoxins correlate with circulating advanced glycation end product levels in renal failure patients
    Jaime Uribarri
    Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Am J Kidney Dis 42:532-8. 2003
    ..Although elevated AGE levels in patients with renal failure have been attributed to impaired renal clearance and increased endogenous AGE formation, recent data suggest an important role for diet as a source of AGEs...
  39. ncbi request reprint Amelioration of oxidant stress by the defensin lysozyme
    Huixian Liu
    Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
    Am J Physiol Endocrinol Metab 290:E824-32. 2006
    ..Thus LZ provides protection against acute and chronic oxidant injury by mechanisms involving suppression of ROS generation and of OS response genes...
  40. pmc Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cells
    Changyong Lu
    Department of Geriatrics and Adult Development, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029, USA
    Proc Natl Acad Sci U S A 101:11767-72. 2004
    ....
  41. pmc Oxidative stress-induced JNK activation contributes to proinflammatory phenotype of aging diabetic mesangial cells
    Jin Wu
    Divison of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Am J Physiol Renal Physiol 297:F1622-31. 2009
    ..Proinflammatory phenotype of mesangial cells may contribute to chronic inflammatory lesions and disease progression of aging diabetic mice...
  42. ncbi request reprint Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products
    Feng Zheng
    Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Diabetes Metab Res Rev 18:224-37. 2002
    ..The relative contribution of diet-derived AGEs to diabetic nephropathy (DN) remains unclear...
  43. ncbi request reprint Advanced glycation end products and diabetic complications: a general overview
    Melpomeni Peppa
    Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, NY, NY 10029, USA
    Hormones (Athens) 4:28-37. 2005
    ....
  44. pmc Advanced glycation end products in foods and a practical guide to their reduction in the diet
    Jaime Uribarri
    Division of Nephrology, Mount Sinai School of Medicine, New York, NY, USA
    J Am Diet Assoc 110:911-16.e12. 2010
    ..The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake...
  45. ncbi request reprint Targeted disruption of Slc19a2, the gene encoding the high-affinity thiamin transporter Thtr-1, causes diabetes mellitus, sensorineural deafness and megaloblastosis in mice
    Kimihiko Oishi
    Department of Pediatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hum Mol Genet 11:2951-60. 2002
    ..Thus, Slc19a2(-/-) mice have provided new insights into the TRMA disease pathogenesis and will provide a tool for studying the role of thiamin homeostasis in diabetes mellitus more broadly...
  46. pmc Lysozyme enhances renal excretion of advanced glycation endproducts in vivo and suppresses adverse age-mediated cellular effects in vitro: a potential AGE sequestration therapy for diabetic nephropathy?
    F Zheng
    Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Mol Med 7:737-47. 2001
    ....
  47. pmc Reduced acute vascular injury and atherosclerosis in hyperlipidemic mice transgenic for lysozyme
    Huixian Liu
    The Brookdale Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
    Am J Pathol 169:303-13. 2006
    ..This effect may be due to the antioxidant properties of LZ, which is possibly linked to the AGE-binding domain region of the molecule...
  48. ncbi request reprint Prevention and reversal of diabetic nephropathy in db/db mice treated with alagebrium (ALT-711)
    Melpomeni Peppa
    Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA
    Am J Nephrol 26:430-6. 2006
    ..Alagebrium (ALT-711) has been shown to improve renal dysfunction in animal models of diabetes...
  49. pmc Restriction of advanced glycation end products improves insulin resistance in human type 2 diabetes: potential role of AGER1 and SIRT1
    Jaime Uribarri
    Department of Medicine, The Mount Sinai School of Medicine, New York, New York, USA
    Diabetes Care 34:1610-6. 2011
    ..Because basal OS in type 2 diabetic patients is influenced by the consumption of AGEs, we examined whether AGE consumption also affects IR and whether AGER1 and SIRT1 are involved...
  50. ncbi request reprint Diabetes-induced oxidative stress and low-grade inflammation in porcine coronary arteries
    Lifeng Zhang
    Department of Surgery, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Circulation 108:472-8. 2003
    ..Accordingly, the mechanisms of abnormal formation of reactive oxygen species and the changes in inflammatory gene expression were examined in diabetic coronary arteries...
  51. ncbi request reprint Prevention Conference VI: Diabetes and Cardiovascular Disease: Writing Group II: pathogenesis of atherosclerosis in diabetes
    Robert H Eckel
    Circulation 105:e138-43. 2002
  52. ncbi request reprint Aging and glycoxidant stress
    Melpomeni Peppa
    Endocrine Unit, 2nd Dept of Internal Medicine Propaedeutic, Research Institute and Diabetes Center, Athens University, Medical School, Athens, Greece
    Hormones (Athens) 7:123-32. 2008
    ..Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies...
  53. doi request reprint Dietary advanced glycation endproducts and oxidative stress: in vivo effects on endothelial function and adipokines
    Alin Stirban
    Diabetes Center North Rhine Westphalia, Bad Oeynhausen, Germany
    Ann N Y Acad Sci 1126:276-9. 2008
    ..The postprandial excursions in glucose, insulin, and triglycerides were similar between both meals. A meal rich in AGEs induces acute endothelial and adipocyte dysfunction. These effects were prevented by changing the cooking method...
  54. ncbi request reprint Diabetes and advanced glycoxidation end products
    Amy G Huebschmann
    Division of General Internal Medicine, Department of Medicine, University of Colorado Denver and Health Sciences Center, Mailstop F 729, Aurora, CO 80045, USA
    Diabetes Care 29:1420-32. 2006
  55. ncbi request reprint Effects of low- and high-advanced glycation endproduct meals on macro- and microvascular endothelial function and oxidative stress in patients with type 2 diabetes mellitus
    Monica Negrean
    Diabetes Clinic, Heart and Diabetes Centre NRW Bad Oeynhausen, Ruhr University Bochum, Germany
    Am J Clin Nutr 85:1236-43. 2007
    ..An advanced glycation endproducts (AGEs)-rich diet induces significant increases in inflammatory and endothelial dysfunction markers in type 2 diabetes mellitus (T2DM)...
  56. ncbi request reprint Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes
    Alin Stirban
    Heart and Diabetes Center NRW, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
    Diabetes Care 29:2064-71. 2006
    ....
  57. ncbi request reprint Glycotoxins: a missing link in the "relationship of dietary fat and meat intake in relation to risk of type 2 diabetes in men"
    Melpomeni Peppa
    Diabetes Care 25:1898-9. 2002

Research Grants20

  1. AGING AND VASCULAR DISEASE: ROLE OF GLYCATION
    Helen Vlassara; Fiscal Year: 2007
    ..diabetes, diet. The proposed studies will expand our understanding of this basic process and may allow us to identify ways to prevent AGE-induced vascular injury due to diabetes and aging. ..
  2. Effects of Glycoxidative Stress on Human Aging
    Helen Vlassara; Fiscal Year: 2010
    ....
  3. Vascular Response and Glycoxidant Homeostasis
    Helen Vlassara; Fiscal Year: 2007
    ..The elucidation of AGER1 mechanisms, which influence the regulation of AGE clearance (positively) and/or the pro-OS, inflammatory pathways (negatively) may generate new therapeutic targets against human vascular disease. ..
  4. Effects of Glycoxidative Stress on Human Aging
    Helen Vlassara; Fiscal Year: 2007
    ..It is hoped that the data will lay the groundwork for future studies evaluating optimal methods of nutrient preparation as ways to ameliorate a major environmental promoter of pro-oxidant events, and thus aging. ..
  5. Vascular Response and Glycoxidant Homeostasis
    Helen Vlassara; Fiscal Year: 2009
    ..The elucidation of AGER1 mechanisms, which influence the regulation of AGE clearance (positively) and/or the pro-OS, inflammatory pathways (negatively) may generate new therapeutic targets against human vascular disease. ..
  6. AGING AND VASCULAR DISEASE--ROLE OF GLYCATION
    Helen Vlassara; Fiscal Year: 2001
    ..Based on the multifaceted properties of the AGE receptor system, these studies should provide a molecular basis for the future epidemiology and treatment of age-related vascular disease. ..
  7. AGE-RECEPTORS AND KIDNEY DISEASE
    Helen Vlassara; Fiscal Year: 2003
    ....