ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 83 citations in OpenAlex.
- Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.Frontiers in immunology · 2026Article
- The interplay of dietary sugar, chronic inflammation, and bladder cancer: mechanistic insights, evidence, and prevention strategies.Frontiers in immunology · 2026Review
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- Engineered metallic hybrid nanozyme for advanced inflammatory disease therapy.Materials today. Bio · 2025Review
- Effects of glutaminase 1 inhibitor on rotator cuff derived cells: a preliminary report in 12 patients.BMC musculoskeletal disorders · 2025Article
- AGEs Inducing EPCs Apoptosis via ROS and p38 MAPK/JNK Pathways in Diabetic Vascular Complications.Physiological research · 2025Article
- rhaFGF promotes acute diabetic wound healing by suppressing chronicity of inflammation.Scientific reports · 2025Article
- Dysfunctional crosstalk between macrophages and fibroblasts under LPS-infected and hyperglycemic environment in diabetic wounds.Scientific reports · 2025Article
- The role of AGEs in skeletal muscle atrophy and the beneficial effects of exercise.Frontiers in medicine · 2025Review
- Innovations in hydrogel therapies for diabetic wound healing: bridging the gap between pathophysiology and clinical application.Burns & trauma · 2025Review
- Fermented Fish Collagen Diminished Photoaging-Related Collagen Decrease by Attenuating AGE-RAGE Binding Activity.Current issues in molecular biology · 2024Article
- Advanced Glycation End-Products Acting as Immunomodulators for Chronic Inflammation, Inflammaging and Carcinogenesis in Patients with Diabetes and Immune-Related Diseases.Biomedicines · 2024Review
- circCDK13-loaded small extracellular vesicles accelerate healing in preclinical diabetic wound models.Nature communications · 2024Article
- Skin advanced glycation end-products as indicators of the metabolic profile in diabetes mellitus: correlations with glycemic control, liver phenotypes and metabolic biomarkers.BMC endocrine disorders · 2024Article
- Combined therapeutic strategy based on blocking the deleterious effects of AGEs for accelerating diabetic wound healing.Regenerative biomaterials · 2024Article
- Intra-articular site-specific distribution of advanced glycation end products in the shoulder of patients with diabetes mellitus having rotator cuff tears.Molecular biology reports · 2023Article
- Staphylococcus aureus enhances osteoclast differentiation and bone resorption by stimulating the NLRP3 inflammasome pathway.Molecular biology reports · 2023Article
- MiR-146a-5p Contributes to Microglial Polarization Transitions Associated With AGEs.Molecular neurobiology · 2023Article
- Antioxidant Activities of Natural Compounds from Caribbean Plants to Enhance Diabetic Wound Healing.Antioxidants (Basel, Switzerland) · 2023Review
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
BACKGROUND Type 2 diabetes impairs the healing process and induces apoptosis of fibroblasts, which are thought to be involved in this process. We investigated the possible mechanisms involved in AGEs-induced apoptosis of human dermal fibroblasts. MATERIAL AND METHODS We examined the expression of apoptosis-related proteins in fibroblasts isolated from human diabetic wounds. Human dermal fibroblasts exposed to AGEs were used to study the links among apoptosis, ROS, and NLRP3 inflammasome activation. Signaling mechanisms were evaluated by preincubating the cells with appropriate inhibitors. Cleaved caspase-8, cleaved caspase-3, BAX, Bcl-2, and NLRP3 inflammasome expression were measured by Western blot analysis. ROS generation, cell viability, and cell apoptosis were assessed. RESULTS We observed a higher level of cleaved caspase-8 and cleaved caspase-3 expression in fibroblasts isolated from human diabetic wounds compared with controls. AGEs decreased the proliferation of cells in a concentration-dependent and time-dependent manner. The exposure of fibroblasts to AGEs significantly increased the number of cells in early and late apoptosis stages. AGES-induced human dermal fibroblasts showed high expressions of cleaved caspase3, cleaved caspase8, and Bax. Treatment with AGEs induced the expression of NLRP3, caspase-1, and ASC. AGES-induced apoptosis was blocked by BAY 11-7082, an inhibitor of the NLRP3 inflammasome. AGEs increased the production of ROS in fibroblasts, and its apoptogenic effect was blocked by NAC. CONCLUSIONS AGEs cause apoptosis of fibroblasts by inducing the generation of ROS and activating the NLRP3 inflammasome. In vivo experiments are needed to confirm these results.
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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.