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Cited by 109Advanced Glycation End Products researchAtherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin Effects

Lowering of dietary advanced glycation endproducts (AGE) reduces neointimal formation after arterial injury in genetically hypercholesterolemic mice

Lin, Reigh-Yi, Reis, Ernane D, Dore, Anthony T, Lu, Min, Ghodsi, Newsha, Fallon, John T, Fisher, Edward A, Vlassara, Helen·2002·Atherosclerosis
DOI 10.1016/s0021-9150(02)00008-4
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Abstract

Restenosis remains a major cause of morbidity and mortality after coronary angioplasty. Injury-induced inflammation, thrombosis, smooth muscle cell (SMC) proliferation, and neointimal formation contribute to restenosis. These events are linked to circulating glucose-derived advanced gycation endproducts (AGE), known to promote cell proliferation, lipid glycoxidation and oxidant stress. This study evaluates the association between dietary AGE content and neointimal formation after arterial injury in genetically hypercholesterolemic mice. Male, 12-week-old, apolipoprotein E-deficient (apoE(-/-)) mice were randomly assigned to receive either a high AGE diet (HAD; AGE=15000 U/mg), or a similar diet with ten-fold lower AGE (LAD; AGE=1500 U/mg). These mice underwent femoral artery injury 1 week later, and were maintained on their diets for an additional 4 weeks. At 4 weeks after injury, significant decrease in neointimal formation was noted in LAD-fed mice. Neointimal area, intima/media ratio, and stenotic luminal area (LA) were less pronounced in the LAD group than the HAD group (P<0.05). These quantitative differences were associated with a marked reduction ( approximately 56%) of macrophages in the neointimal lesions, as well as an obvious reduction of SMC content of LAD-fed mice. The reduction of neointimal formation in the LAD mice correlated with a approximately 40% decrease in circulating AGE levels (P<0.0005). Immunohistochemistry also showed a reduced ( approximately 1.5-fold) deposition of AGE in the endothelia, SMC, and macrophages in neointimal lesions of LAD-fed mice. These results represent the first evidence in vivo for a causal relationship between dietary AGE and the vessel wall response to acute injury, suggesting a significant potential for dietary AGE restriction in the prevention of restenosis after angioplasty.

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  • Cytokine-induced SOCS1 and SOCS3 prevent tyrosine phosphorylation of IRS proteins by direct interference or ubiquitylation/degradation.

    “Another mechanism involves cytokine-induced suppressor of cytokine signalling 1 and 3, which also prevent tyrosine phosphorylation of IRS proteins, by direct interference, or ubiquitylation and subsequent degradation (130,131) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [131]

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Authors
Lin, R.-Y., Reis, E. D., Dore, A. T., Lu, M., Ghodsi, N., Fallon, J. T., Fisher, E. A., & Vlassara, H.
Affiliations
  • Icahn School of Medicine at Mount Sinai (US)
  • Mount Sinai Hospital (US)
Corresponding author
Lin, Reigh-Yi
ORCID
Venue
Atherosclerosis
Publisher
Elsevier BV
Published
2002-08
Volume
163
Issue
2
Pages
303-311
ISSN
0021-9150 (ISSN-L)
DOI
10.1016/s0021-9150(02)00008-4
OpenAlex
W2021001924
Cited by
109
References
33
Citations by year
2026: 1 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 2 · 2017: 2 · 2016: 5 · 2015: 8 · 2014: 1 · 2013: 6 · 2012: 3
FWCI
5.19
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Atherosclerosis (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG09453, R01AG009453)
  • National Heart, Lung, and Blood Institute (R01HL061814, HL61814)
  • National Institute of Diabetes and Digestive and Kidney Diseases (T32DK007645, DK07645)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
advanced glycation end products, neointima formation, restenosis, arterial injury, hypercholesterolemia, ApoE-deficient mice, smooth muscle cell proliferation, macrophages, angioplasty complications
MeSH terms
Animals, Constriction, Pathologic, Dietary Carbohydrates, Femoral Artery, Hyperlipoproteinemia Type II, Hyperplasia, Male, Mice, Inbred C57BL, Glycation End Products, Advanced, Tunica Intima, Mice

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