ArticleInternational urogynecology journal2022
The polymorphisms of extracellular matrix-remodeling genes are associated with pelvic organ prolapse.
Article in International urogynecology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 12 citations in OpenAlex.
- Pelvic Organ Prolapse with an Emphasis on the Central Compartment: From Genetic Risk Factors and Biomarkers to Contemporary Sacropexy and Emerging Robotic Innovations.Journal of clinical medicine · 2026Review
- Network-informed multi-trait genomic analysis decodes the shared genetic architecture and therapeutic landscape of pelvic floor disorders.npj aging · 2026Article
- Insights into risk factors and interactive effects on epiretinal membrane development from the National Health and Nutrition Examination Survey.International journal of ophthalmology · 2026Article
- 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
- Effects of Urinary Incontinence Subtypes on Quality of Life and Sexual Function among Women Seeking Weight Loss.International urogynecology journal · 2025Article
- Anatomo-pathological aspects of pelvic organ prolapse: analytical study of round and utero-sacral ligaments of Congolese women during the mass campaign in two hospitals of city of Kananga.The Pan African medical journal · 2025Article
- Impact of Milk Consumption and Dietary Patterns on Pelvic Organ Prolapse: A Mendelian Randomization Study.International journal of women's health · 2025Article
- Expression level of matrix metalloproteinases -1, -2 and -9 associated with pelvic organ prolapse: experimental analytical study of round ligaments of Congolese women in two hospitals from the city of Kananga in Democratic Republic of Congo.The Pan African medical journal · 2025Article
- Association between TGF-β1 and β-catenin expression in the vaginal wall of patients with pelvic organ prolapse.Open life sciences · 2025Article
- Review
- Exosomes derived from mesenchymal stromal cells: a promising treatment for pelvic floor dysfunction.Human cell · 2023Review
- Long-term menopause exacerbates vaginal wall support injury in ovariectomized rats by regulating amino acid synthesis and glycerophospholipid metabolism.Frontiers in endocrinology · 2023Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
introduction and hypothesisExtracellular matrix (ECM) synthesis and metabolism abnormalities may influence the pelvic supporting system and lead to the occurrence and development of pelvic organ prolapse (POP). Genetic polymorphisms of such related genes have been increasingly studied. This study aims to explore the association between the single-nucleotide polymorphisms (SNPs) of genes encoding ECM processing enzymes (a disintegrin and metalloproteinase with thrombospondin motifs [ADAMTSs]), ECM degrading enzymes (matrix metalloproteinases [MMPs]) and their tissue inhibitors of metalloproteinase (TIMPs), and POP.
methodsWe conducted an association study including 48 women with POP at stages III and IV and 48 women without prolapse in Chinese groups. SNPs were identified using the target region sequencing technique. We performed Fisher's exact tests to assess the association between SNPs and POP in the unadjusted model and logistic regression analysis in the adjusted model, adjusting for delivery and pregnancy.
resultsThere was a significant association between TIMP2 SNP rs2277698 (odds ratio [OR], 0.37; 95% confidence interval [CI], 0.16-0.82; P = 0.015), ADAMTS13 SNP rs149586801 (OR, 0.18; 95% CI, 0.05-0.69; P = 0.012), and ADAMTS1 SNPs rs370850 and rs422803 (OR, 3.71; 95% CI, 1.35-10.15; P = 0.011 for both), rs402007, rs428785, rs434857, and rs445784 (OR, 2.18; 95% CI, 1.05-4.56; P = 0.038 for the four), and POP in the adjusted model.
conclusionTIMP2, ADAMTS13, and ADAMTS1 might be candidate genes for POP. Our results provide preliminarily new evidence for future investigation of these genes in the pathophysiology of POP.
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