ArticleRespiratory research2016
Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis.
Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
- Activating the Osteoblastic USP26 Pathway Alleviates Multi-Organ Fibrosis by Decreasing Insulin Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The AGE-RAGE Pathway in Endometriosis: A Focused Mechanistic Review and Structured Evidence Map.International journal of molecular sciences · 2026Review
- Skin advanced glycation end-products do not predict pulmonary function trajectories in adults from the ILERVAS cohort.Scientific reports · 2026Article
- Connecting sugar and fibrosis: Diabetes as a hidden player in rheumatoid arthritis-associated interstitial lung disease.World journal of clinical cases · 2026Article
- Association between hemoglobin glycation index and mortality in critically ill patients with chronic obstructive pulmonary disease: a retrospective cohort study.European journal of medical research · 2026Article
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- A bovine pulmosphere model and multiomics reveal early host response signature in tuberculosis.Communications biology · 2025Article
- Reversing Oxinflammation Associated with Glycative Stress and Formation of Advanced Glycation End Products with a Dietary Supplement Containing Rosemary Extract.The Journal of clinical and aesthetic dermatology · 2025Article
- Qimai Feiluoping Decoction Inhibits EndMT to Alleviate Pulmonary Fibrosis by Reducing PI3K/AKT/mTOR Pathway-Mediated the Restoration of Autophagy.Journal of inflammation research · 2025Article
- Identification of diagnostic hub genes related to energy metabolism in idiopathic pulmonary fibrosis.Frontiers in molecular biosciences · 2025Article
- Identifying Mechanism of Resveratrol for the Treatment of COVID-19 and Idiopathic Pulmonary FibrosisCurrent medicinal chemistry · 2025Article
- Altered expression pattern of immune response-related genes and isoforms in hypersensitivity pneumonitis lung fibroblasts.Scientific reports · 2024Article
- Article
- The TOX-RAGE axis mediates inflammatory activation and lung injury in severe pulmonary infectious diseases.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Elucidating shared biomarkers in gastroesophageal reflux disease and idiopathic pulmonary fibrosis: insights into novel therapeutic targets and the role of angelicae sinensis radix.Frontiers in pharmacology · 2024Article
- Nε-Carboxymethyl-Lysine Modification of Extracellular Matrix Proteins Augments Fibroblast Activation.International journal of molecular sciences · 2023Article
- The Remarkable Roles of the Receptor for Advanced Glycation End Products (RAGE) and Its Soluble Isoforms in COVID-19: The Importance of RAGE Pathway in the Lung Injuries.Indian journal of clinical biochemistry : IJCB · 2023Review
- Diagnosis of Fibrotic Hypersensitivity Pneumonitis: Is There a Role for Biomarkers?Life (Basel, Switzerland) · 2023Review
- Diabetic endothelial microangiopathy and pulmonary dysfunction.Frontiers in endocrinology · 2023Review
- Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome.Life (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe abnormal epithelial-mesenchymal restorative capacity in idiopathic pulmonary fibrosis (IPF) has been recently associated with an accelerated aging process as a key point for the altered wound healing. The advanced glycation end-products (AGEs) are the consequence of non-enzymatic reactions between lipid and protein with several oxidants in the aging process. The receptor for AGEs (RAGEs) has been implicated in the lung fibrotic process and the alveolar homeostasis. However, this AGE-RAGE aging pathway has been under-explored in IPF.
methodsLung samples from 16 IPF and 9 control patients were obtained through surgical lung biopsy. Differences in AGEs and RAGE expression between both groups were evaluated by RT-PCR, Western blot and immunohistochemistry. The effect of AGEs on cell viability of primary lung fibrotic fibroblasts and alveolar epithelial cells was assessed. Cell transformation of fibrotic fibroblasts cultured into glycated matrices was evaluated in different experimental conditions.
resultsOur study demonstrates an increase of AGEs together with a decrease of RAGEs in IPF lungs, compared with control samples. Two specific AGEs involved in aging, pentosidine and Nε-Carboxymethyl lysine, were significantly increased in IPF samples. The immunohistochemistry identified higher staining of AGEs related to extracellular matrix (ECM) proteins and the apical surface of the alveolar epithelial cells (AECs) surrounding fibroblast foci in fibrotic lungs. On the other hand, RAGE location was present at the cell membrane of AECs in control lungs, while it was almost missing in pulmonary fibrotic tissue. In addition, in vitro cultures showed that the effect of AGEs on cell viability was different for AECs and fibrotic fibroblasts. AGEs decreased cell viability in AECs, even at low concentration, while fibroblast viability was less affected. Furthermore, fibroblast to myofibroblast transformation could be enhanced by ECM glycation.
conclusionsAll of these findings suggest a possible role of the increased ratio AGEs-RAGEs in IPF, which could be a relevant accelerating aging tissue reaction in the abnormal wound healing of the lung fibrotic process.
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