TGFB2-mediated regeneration of pelvic ligament equivalents using a stem cell-fibroblast-decellularized membrane composite.
Dong Y., Zhang Y., Duan Y., Xia Z.
Laboratory Study on Ligament Injury, published in Front Bioeng Biotechnol (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Front Bioeng Biotechnol (2026)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42564500
- DOI
- 10.3389/fbioe.2026.1763991
Abstract (original English)
Pelvic organ prolapse (POP) is a prevalent condition characterized by weakened pelvic floor tissues, significantly impacting women's quality of life. Current treatments, including synthetic meshes and native tissue repair, face challenges of high recurrence rates and complications. This study developed a novel tissue-engineered strategy utilizing a decellularized human amniotic membrane (HAAM) scaffold seeded with autologous adipose-derived mesenchymal stem cells (ADSCs) and vaginal wall fibroblasts (HVFs) to construct a bioactive pelvic ligament equivalent. We first validated the successful preparation of HAAM with preserved extracellular matrix integrity and characterized the phenotypic markers of ADSCs and HVFs. In a rat abdominal wall defect model, the HAAM+ADSCs+HVFs composite demonstrated superior tissue regeneration and integration, reduced fibrosis, and effective modulation of the host immune microenvironment -evidenced by enhanced repair and decreased infiltration of pro-inflammatory cells -compared to all control groups (including HAAM alone and single-cell groups). Transcriptomic analysis revealed that the composite treatment promoted extracellular matrix organization and collagen synthesis while suppressing matrix degradation (MMP2/MMP9) and inflammatory pathways. Most importantly, mechanistic studies identified TGFB2 as the key paracrine mediator through which ADSC
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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