ReviewCardiovascular diabetology2015
Crosstalk between advanced glycation end products (AGEs)-receptor RAGE axis and dipeptidyl peptidase-4-incretin system in diabetic vascular complications.
Review in Cardiovascular diabetology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 121 citations in OpenAlex.
- Combined effect of metformin with ascorbic acid versus acetyl salicylic acid on diabetes-related cardiovascular complication; a 12-month single blind multicenter randomized control trial.Cardiovascular diabetology · 2017 · on this mapTrial
- Multi-trajectories of serum uric acid/high density lipoprotein cholesterol ratio and fasting plasma glucose in chronic kidney disease.Annals of medicine · 2026Article
- Effects of the glucagon-like peptide-1 receptor agonist PEG-Loxe on diabetic osteoporosis: A mechanistic study.Molecular metabolism · 2026Article
- Potential for anti‑angiogenic therapy targeting the receptor for advanced glycation end products/VEGF axis in ulcerative colitis (Review).Molecular medicine reports · 2026Review
- Hyperglycaemia-induced molecular reprogramming of proximal tubular epithelial cells and its contribution to diabetic kidney disease progression-a narrative review.Frontiers in cell and developmental biology · 2026Review
- The effects of DPP4 inhibitors, SGLT2 inhibitors and GLP1-RA on the AGE/RAGE pathway: implications for diabetes and its complications.Glycoconjugate journal · 2025Review
- Paracrine Signaling by Distinct Adipose Tissue Depots Regulate Fibroblast Mechanobiology and Functional Heterogeneity.Cellular and molecular bioengineering · 2025Article
- AGEs Inducing EPCs Apoptosis via ROS and p38 MAPK/JNK Pathways in Diabetic Vascular Complications.Physiological research · 2025Article
- Crosstalk Between Metabolic Biomarkers and Pulse Wave Analysis in Hypertensive Patients.Biomedicines · 2025Article
- Rhamnan Sulfate from the SeaweedMarine drugs · 2025Article
- Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications.International journal of molecular sciences · 2025Review
- Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024Review
- New Insights into the Pleiotropic Actions of Dipeptidyl Peptidase-4 Inhibitors Beyond Glycaemic Control.TouchREVIEWS in endocrinology · 2024Review
- Advancements in diabetic foot ulcer research: Focus on mesenchymal stem cells and their exosomes.Heliyon · 2024Review
- Polysaccharides from Seedless Chestnut Rose (Foods (Basel, Switzerland) · 2024Article
- METTL3-mediated NDUFB5 m6A modification promotes cell migration and mitochondrial respiration to promote the wound healing of diabetic foot ulcer.Journal of translational medicine · 2024Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Profile analysis of differentially expressed long non‑coding RNAs in metabolic memory induced by high glucose in human umbilical vein endothelial cells.Experimental and therapeutic medicine · 2023Article
- Insights on the role of anti-inflammatory and immunosuppressive agents in the amelioration of diabetes.Diabetology international · 2023Review
- Potential Mechanisms of Yiqi Jiedu Huayu Decoction in the Treatment of Diabetic Microvascular Complications Based on Network Analysis, Molecular Docking, and Experimental Validation.Evidence-based complementary and alternative medicine : eCAM · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs) consist of heterogenous group of macroprotein derivatives, which are formed by non-enzymatic reaction between reducing sugars and amino groups of proteins, lipids and nucleic acids, and whose process has progressed at an accelerated rate under diabetes. Non-enzymatic glycation and cross-linking of protein alter its structural integrity and function, contributing to the aging of macromolecules. Furthermore, engagement of receptor for AGEs (RAGE) with AGEs elicits oxidative stress generation and subsequently evokes proliferative, inflammatory, and fibrotic reactions in a variety of cells. Indeed, accumulating evidence has suggested the active involvement of accumulation of AGEs in diabetes-associated disorders such as diabetic microangiopathy, atherosclerotic cardiovascular diseases, Alzheimer's disease and osteoporosis. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretins, gut hormones secreted from the intestine in response to food intake, both of which augment glucose-induced insulin release, suppress glucagon secretion, and slow gastric emptying. Since GLP-1 and GIP are rapidly degraded and inactivated by dipeptidyl peptidase-4 (DPP-4), inhibition of DPP-4 and/or DPP-4-resistant GLP-1 analogues have been proposed as a potential target for the treatment of diabetes. Recently, DPP-4 has been shown to cleave multiple peptides, and blockade of DPP-4 could exert diverse biological actions in GLP-1- or GIP-independent manner. This article summarizes the crosstalk between AGEs-RAGE axis and DPP-4-incretin system in the development and progression of diabetes-associated disorders and its therapeutic intervention, especially focusing on diabetic vascular complications.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.