ReviewGlycoconjugate journal2016
Systemic effects of AGEs in ER stress induction in vivo.
Review in Glycoconjugate journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- CNTN-1 regulates malignant biological behaviors of lung squamous cell carcinoma (LUSC) via the endoplasmic reticulum stress (ERS)/epithelial-mesenchymal transition (EMT) axis.Translational cancer research · 2026Article
- Exosomal miR-221-3p derived from bone marrow mesenchymal stem cells alleviates endoplasmic reticulum stress-mediated apoptosis in nucleus pulposus cells via the Nrf2/HO-1 signalling pathway.International journal of experimental pathology · 2025Article
- Advanced Glycation End Products Induce Caudal Disc Degeneration in Ovariectomized Female Rats.JOR spine · 2025Article
- The endoplasmic reticulum stress-related genes and molecular typing predicts prognosis and reveals characterization of tumor immune microenvironment in lung squamous cell carcinoma.Discover oncology · 2024Article
- Achilles' Heel-The Significance of Maintaining Microenvironmental Homeostasis in the Nucleus Pulposus for Intervertebral Discs.International journal of molecular sciences · 2023Review
- Article
- LCZ696 Protects against Diabetic Cardiomyopathy-Induced Myocardial Inflammation, ER Stress, and Apoptosis through Inhibiting AGEs/NF-κB and PERK/CHOP Signaling Pathways.International journal of molecular sciences · 2022Article
- Ischemic brain injury in diabetes and endoplasmic reticulum stress.Neurochemistry international · 2022Review
- Comprehensive Analysis of the Clinical and Biological Significances of Endoplasmic Reticulum Stress in Diffuse Gliomas.Frontiers in cell and developmental biology · 2021Article
- Exosomes Immunity Strategy: A Novel Approach for Ameliorating Intervertebral Disc Degeneration.Frontiers in cell and developmental biology · 2021Review
- Investigation of diabetic patient's fingernail quality to monitor type 2 diabetes induced tissue damage.Scientific reports · 2019Article
- Article
- Mechanistic targeting of advanced glycation end-products in age-related diseases.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression.Scientific reports · 2018Article
- Maternal intake of fried foods and risk of gestational diabetes mellitus.Annals of epidemiology · 2017Article
- Advanced glycation end products promote the proliferation and migration of primary rat vascular smooth muscle cells via the upregulation of BAG3.International journal of molecular medicine · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence indicates that accumulation of advanced glycation end products (AGEs) in human tissues may contribute to cell injury, inflammation and apoptosis through induction of endoplasmic reticulum (ER) stress. Human metabolism relies on ER homeostasis for the coordinated response of all metabolic organs by controlling the synthesis and catabolism of various nutrients. In vitro studies have demonstrated AGE-induced enhancement of unfolded protein response (UPR) in different cell types including endothelial, neuronal, pancreatic cells and podocytes, suggesting this crosstalk as an underlying pathological mechanism that contributes to metabolic diseases. In this minireview, we describe in vivo studies undertaken by our group and others that demonstrate the diverse systemic effects of AGEs in ER stress induction in major metabolic tissues such as brain, kidney, liver and pancreas of normal mice. Administration of high-AGEs content diet to normal mice for the period of 4 weeks upergulates the mRNA and protein levels of ER chaperone Bip (GRP78) indicative of UPR initiation in all major metabolic organs and induces activation of the pivotal transcription factor XBP1 that regulates glucose and lipid metabolism. Furthermore, animals with genetic ablation of UPR-activated transcription factor C/EBP homologous protein CHOP allocated in high-AGEs diet, exhibited relative resistance to UPR induction (BiP levels) and XBP1 activation in major metabolic organs. Since CHOP presents a critical mediator that links accumulation and aggregation of unfolded proteins with induction of oxidative stress and ER stress-related apoptosis, it is revealed as an important molecular target for the management of metabolic diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.