ArticleInternational urogynecology journal2024
Mechanical Stress-Oxidative Stress Axis: Biological Basis in the Vaginal Wall and Pelvic Floor Muscles of Rats with Simulated Birth Injury.
Article in International urogynecology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Thrombospondin-1 as a Mechanosensitive Matrix Protein Driving Fibroblast Senescence: A Novel Pathogenic Target for Pelvic Organ Prolapse.International urogynecology journal · 2026Article
- Recombinant Humanized Collagen: A Promising Treatment for Pelvic Organ Prolapse via Enhanced Fibroblast Function and Angiogenesis.International urogynecology journal · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
introduction and hypothesisVaginal delivery and resulting pelvic floor muscle (PFM) dysfunction are significant risk factors for pelvic floor dysfunction (PFD). Despite this, the biological basis underlying PFD after childbirth remain unclear. This study was aimed at assessing the early response of the vaginal wall and PFM to simulated birth injury (SBI) in rats.
methodsForty female Sprague-Dawley rats were divided into four groups: control (sham operation), and 1, 4, and 14 days post-injury. In the SBI groups, a catheter was inserted into the vagina with 130 g of weight attached to the end, and the balloon was inflated to 5 ml for 2 h. Evaluation of vaginal tissues and PFMs included histological, immunohistochemical, Western blot, and uniaxial biomechanical testing.
resultsIn the vaginal wall, the SBI group showed significantly lower COL1A1 expression and higher MMP-2 and MMP-9 expression. At 4 and 14 days post-injury, there was a significant decrease in PFM fiber area and increased collagen content. The SBI group also exhibited significant increases in the expression of Nrf2, NQO1, HO-1, and SOD-2, indicating involvement of oxidative stress in both the vaginal wall and PFMs. Protein expression of Pax7 and MyoG, as well as the number of fibers with centralized nuclei, continued to increase significantly after SBI. Additionally, the vaginal wall of the SBI group showed a decreasing trend in tensile strength and elastic modulus, with a greater ultimate strain.
conclusionExtracellular matrix remodeling, oxidative stress, decreased biomechanical properties, and muscle dysmyogenesis may collectively contribute to increased susceptibility to PFD development.
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