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Glycoconjugate Journal

, Volume 35, Issue 5, pp 443–450 | Cite as

Role of AGEs in the progression and regression of atherosclerotic plaques

  • Zhong-qun Wang
  • Le-le Jing
  • Jin-chuan Yan
  • Zhen Sun
  • Zheng-yang Bao
  • Chen Shao
  • Qi-wen Pang
  • Yue Geng
  • Li-li Zhang
  • Li-hua Li
Review Article

Abstract

The formation of advanced glycation end-products(AGEs) is an important cause of metabolic memory in diabetic patients and a key factor in the formation of atherosclerosis(AS) plaques in patients with diabetes mellitus. Related studies showed that AGEs could disrupt hemodynamic steady-state and destroy vascular wall integrity through the endothelial barrier damage, foam cell(FC) formation, apoptosis, calcium deposition and other aspects. At the same time, AGEs could initiate oxidative stress and inflammatory response cascade via receptor-depended and non-receptor-dependent pathways, promoting plaques to develop from a steady state to a vulnerable state and eventually tend to rupture and thrombosis. Numerous studies have confirmed that these pathological processes mentioned above could lead to acute coronary heart disease(CHD) and other acute cardiovascular and cerebrovascular events. However, the specific role of AGEs in the progression and regression of AS plaques has not yet been fully elucidated. In this paper, the formation, source, metabolism, physical and chemical properties of AGEs and their role in the migration of FCs and plaque calcification are briefly described, we hope to provide new ideas for the researchers that struggling in this field.

Keywords

Advanced glycation end-products Foam cell migration Plaque calcification Atherosclerosis 

Abbreviations

AGEs

advanced glycation end-products

AS

atherosclerosis

FC

foam cell

CHD

coronary heart disease

VC

vascular calcification

VSMC

vascular smooth muscle cell

AB

apoptotic body

CML

Nε-Carboxymethyllysine

Notes

Availability of data and materials

Not applicable.

Authors’ contributions

All authors contributed to conception and design and wrote the review; All authors read and approved the final manuscript.

Fundings

This work was supported by the National Natural Science Foundation of China (Grant Nos. 81770450, 81370408, 81670105); Jiangsu Provincial Health and Family Planning Commission project(QNRC2016836); the Open Program of Key Laboratory of Nuclear Medicine, Ministry of Health and Jiangsu Key Laboratory of Molecular Nuclear Medicine(KF201504); Innovation plan for postgraduate research in Jiangsu Province(KYCX17_1801).

Compliance with ethical standards

Conflicts of interest

The authors declare that they have no competing interests.

Ethical approval

Not applicable.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Zhong-qun Wang
    • 1
  • Le-le Jing
    • 1
  • Jin-chuan Yan
    • 1
  • Zhen Sun
    • 1
  • Zheng-yang Bao
    • 1
  • Chen Shao
    • 1
  • Qi-wen Pang
    • 1
  • Yue Geng
    • 1
  • Li-li Zhang
    • 1
  • Li-hua Li
    • 2
  1. 1.Department of CardiologyAffiliated Hospital of Jiangsu UniversityZhenjiangChina
  2. 2.Department of PathologyAffiliated Hospital of Jiangsu UniversityZhenjiangChina

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