Involvement of Advanced Glycation End Products in the Pathogenesis of Diabetic Retinopathy
Open accessAbstract
Diabetic retinopathy (DR) is a common and devastating microvascular complication of diabetes and a major cause of acquired blindness in young adults. Advanced glycation end products (AGEs) accumulated under hyperglycemic conditions are thought to play an important role in the pathogenesis of DR. AGEs can exert their deleterious effects by acting directly to induce aberrant crosslinking of extracellular matrix proteins, to increase vascular stiffness, altering vascular structure and function. Moreover, AGEs binding to the receptor for AGEs (RAGE) evokes intensive intracellular signaling cascades that leading to endothelial dysfunction, elaboration of key proinflammatory cytokines and proangiogenic factors, mediating pericyte apoptosis, vascular inflammation and angiogenesis, as well as breakdown of the inner blood-retinal barrier (BRB), the end result of all these events is damage to the neural and vascular components of the retina. Elucidation of AGE-induced mechanisms will help in the understanding of the complex cellular and molecular pathogenesis associated with DR. Novel anti-AGEs agents or AGE crosslink “breakers” are being investigated, it is hoped that in next few years, some of these promising therapies will be successfully applied in clinical context, aiming to reduce the major economical and medical burden caused by DR.
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In blood vessels, accumulated AGEs interact with mononuclear, endothelial, and smooth muscle cells, resulting in cellular dysfunction, tissue damage, and atherosclerosis development.
“In blood vessels, accumulated AGEs also interact with mononuclear, endothelial, and smooth muscle cells, resulting in cellular dysfunction, tissue damage, and atherosclerosis development55–57,59.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
AGEs play important roles in diabetic microvascular complications by cross-linking with extracellular matrix proteins, altering vascular elasticity, structure, and function.
“AGEs play important roles in diabetic microvascular complications by cross-linking with extracellular matrix proteins, thereby altering vascular elasticity, structure, and function56.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
Accumulation and exposure to AGEs exacerbate oxidative stress and inflammation and initiate the oxidation of LDLs, which are harmful to cardiovascular function.
“The accumulation and exposure to AGEs exacerbate oxidative stress and inflammation and initiate the oxidation of low-density lipoproteins (LDLs), which are harmful to cardiovascular function.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
The AGE-RAGE interaction instigates pericyte apoptosis, vascular inflammation and permeability, and blood-tissue barrier breakdown.
“In addition, the AGE-RAGE interaction further instigates pericyte apoptosis, vascular inflammation and permeability, and blood-tissue barrier breakdown56.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
Endogenous and exogenous AGEs provoke the initiation and progression of NAFLD, and dietary AGEs from fructose- or sucrose-enriched diets and/or soft drinks can worsen liver fibrosis faster than endogenous AGEs.
“Endogenous and exogenous AGEs provoke the initiation and progression of NAFLD.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
Aggregation of AGEs decreases GSH, SIRT1, and TIMP3 and increases oxidative stress and inflammation, promoting inflammatory liver injury and fibrosis in experimental animal models and NAFLD patients.
“The aggregation of AGEs decreases the levels of the most important cellular antioxidant peptides, glutathione (GSH), SIRT1, and tissue inhibitor of metalloproteinase 3 (TIMP3), accompanied by increased oxidative stress and inflammation, promoting inflammatory liver injury and fibrosis in experimental animal models and NAFLD patients55–57,124–126.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [56]
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- Authors
- Xu, J., Chen, L.-J., Yu, J., Wang, H.-J., Zhang, F., Liu, Q., & Wu, J.
- Affiliations
- Nanfang Hospital (CN)
- Venue
- Cellular Physiology and Biochemistry
- Publisher
- S. Karger AG
- Published
- 2018
- Volume
- 48
- Issue
- 2
- Pages
- 705-717
- ISSN
- 1015-8987 (ISSN-L)
- 1421-9778
- OpenAlex
- W2883415922
- Cited by
- 204
- References
- 73
- Citations by year
- 2026: 13 · 2025: 28 · 2024: 21 · 2023: 28 · 2022: 35 · 2021: 33 · 2020: 31 · 2019: 14 · 2018: 1
- FWCI
- 15.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cellular Physiology and Biochemistry (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Science and Technology Planning Project of Guangdong Province
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Keywords
- diabetic retinopathy, advanced glycation end products, receptor for advanced glycation end products, hyperglycemia, extracellular matrix cross-linking, vascular stiffness, endothelial dysfunction, pericyte apoptosis, angiogenesis, vascular inflammation, blood-retinal barrier breakdown, retinal microvascular complications
- MeSH terms
- Receptor for Advanced Glycation End Products, Blood-Retinal Barrier, Diabetic Retinopathy, Humans, Glycation End Products, Advanced, Reactive Oxygen Species, Vascular Endothelial Growth Factor A, Endoplasmic Reticulum Stress, Tight Junction Proteins
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