Integrated 'Shield-Spear' Biological Patch for Fibrosis-Free Bladder Reconstruction
Wu X., Ruan H., Zhang X., Zheng W., Mutailifu M., Wang L.
Animal Study on Chronic Wound, published in Adv Sci (Weinh) (2025) — 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
- Animal Study
- Journal
- Adv Sci (Weinh) (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40801503
- PMCID
- PMC12591207
- DOI
- 10.1002/advs.202503975
- Citations
- 1
Abstract (original English)
Bladder reconstruction without fibrosis remains a global challenge. Current bladder defect treatments primarily focus on repair at the level of vascularization, failing to balance healing and excessive collagen deposition, and neglecting the exacerbation of fibrosis due to neural dysregulation. In this study, an integrated 'shield-spear' patch composed of an anionic 'shield' hydrogel (HAD) and neuro-targeted 'spear' engineered extracellular vesicles (S100Aptamer-EVs) using Schiff base chemistry and Michael addition reactions is engineered. This novel approach represents the first attempt to synergistically balance the contradiction between fibrosis and wound healing through the 'shield-spear' strategy, achieving extensive bladder reconstruction without fibrosis. In a large animal model of beagles, the outer layer of the 'shield-spear' patch acts as an anionic shield, neutralizing scavenger receptors and selectively capturing GATA6 + peritoneal macrophages to suppress collagen overexpression. The inner layer enables the unidirectional release of S100AptEVs, targeting the activation of Schwann cells to express the brain-derived neurotrophic factor neuroprotective factor, downregulating the TGFβ/Smad fibrosis pathway, thereby collaboratively inhibiting neurogenic fibrosis and activating Cadherin signaling to promote wound healing. The integrated 'shield-spear' patch facilitated su
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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