ArticleInternational journal of molecular medicine2017
Advanced glycation end products decrease collagen I levels in fibroblasts from the vaginal wall of patients with POP via the RAGE, MAPK and NF-κB pathways.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Is there an association between pelvic organ prolapse and oxidative stress? A systematic review.PloS one · 2022Pooled it
- Mechanobiological Dysregulation of Fibroblasts and Extracellular Matrix Failure in Pelvic Organ Prolapse.International urogynecology journal · 2026Review
- RAGE-Mediated Signalling in Gynaecological Disorders: Review of Molecular Mechanisms and Therapeutic Perspectives.Expert reviews in molecular medicine · 2026Review
- Association between glucose and lipid metabolism-related indicators and the occurrence and severity of pelvic organ prolapse in postmenopausal women.Frontiers in medicine · 2026Article
- Multidimensional regulation of estrogen signaling in pelvic floor connective tissue homeostasis and remodeling.Frontiers in immunology · 2026Review
- Noninvasive assessment of oxidative stress in pelvic organ prolapse: a feasibility study.Scientific reports · 2025Article
- Histological and transcriptomic analysis of paravaginal and central defects in anterior vaginal wall prolapse: Insights from DeLancey's pelvic floor theory.Histology and histopathology · 2025Article
- Unveiling the depths of pelvic organ prolapse: From risk factors to therapeutic methods (Review).Experimental and therapeutic medicine · 2025Review
- Genetics of Female Pelvic Organ Prolapse: Up to Date.Biomolecules · 2024Review
- Epithelial-Mesenchymal Transition in Chronic Rhinosinusitis.Journal of rhinology : official journal of the Korean Rhinologic Society · 2024Review
- Role of umbilical cord mesenchymal stromal cells in skin rejuvenation.NPJ Regenerative medicine · 2024Review
- Integration of molecular docking, molecular dynamics and network pharmacology to explore the multi-target pharmacology of fenugreek against diabetes.Journal of cellular and molecular medicine · 2023Article
- Exosomes derived from mesenchymal stromal cells: a promising treatment for pelvic floor dysfunction.Human cell · 2023Review
- Potential molecular targets for intervention in pelvic organ prolapse.Frontiers in medicine · 2023Review
- Advanced glycation end products (AGEs) downregulate the miR-4429/PTEN axis to promote apoptosis of fibroblasts in pelvic organ prolapse.Annals of translational medicine · 2022Article
- Review
- Evaluating the role of type 2 diabetes mellitus in rotator cuff tendinopathy: Development and analysis of a novel rat model.Frontiers in endocrinology · 2022Article
- Advanced glycation end productions and tendon stem/progenitor cells in pathogenesis of diabetic tendinopathy.World journal of stem cells · 2021Review
- Glycation by glyoxal leads to profound changes in the behavior of dermal fibroblasts.BMJ open diabetes research & care · 2021Article
- Single-cell transcriptome profiling of the vaginal wall in women with severe anterior vaginal prolapse.Nature communications · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was carried out to observe the impact of advanced glycation end products (AGEs) on collagen I derived from vaginal fibroblasts in the context of pelvic organ prolapse (POP), and explore the downstream effects on MAPK and nuclear factor-κB (NF-κB) signaling. After treating primary cultured human vaginal fibroblasts (HVFs) derived from POP and non-POP cases with AGEs, cell counting was carried out by sulforhodamine B. The expression levels of collagen I, receptor of advanced glycation end products (RAGE), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were detected by western blot analysis and PCR. RAGE, MAPK and NF-κB were molecularly and pharmacologically-inhibited by siRNA, SB203580 and PDTC, respectively, and downstream changes were detected by western blot analysis and PCR. Inhibition of HVF proliferation by AGEs occurred more readily in POP patients than that noted in the controls. After treatment with AGEs, collagen I levels decreased and MMP-1 levels increased to a greater extent in the HVFs of POP than that noted in the controls. During this same period, RAGE and TIMP-1 levels remained stable. Following treatment with AGEs and RAGE pathway inhibitors by siRNA, SB203580 and PDTC, the impact induced by AGEs was diminished. The inhibition of p-p38 MAPK alone was not able to block the promoting effect of AGEs on the levels of NF-κB, which suggests that AGEs may function through other pathways, as well as p-p38 MAPK. On the whole, this study demonstrated that AGEs inhibited HVF proliferation in POP cases and decreased the expression of collagen I through RAGE and/or p-p38 MAPK and NF-κB-p-p65 pathways. Our results provide important insights into the collagen I metabolism in HVFs in POP.
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