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基于体温诱导水凝胶收缩的皮肤应激屏蔽平台,用于促进无疤痕伤口愈合。

A Skin Stress Shielding Platform Based on Body Temperature-Induced Shrinking of Hydrogel for Promoting Scar-Less Wound Healing.

机构信息

College of Polymer Science and Engineering, State Key Laboratory of Polymer Materials Engineering, Sichuan University, Chengdu, 610065, China.

West China Hospital, Sichuan University/West China School of Nursing, Sichuan University, Chengdu, 610041, China.

出版信息

Adv Sci (Weinh). 2024 Nov;11(41):e2306018. doi: 10.1002/advs.202306018. Epub 2024 Sep 16.

DOI:10.1002/advs.202306018
PMID:39283032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11538717/
Abstract

Stress concentration surrounding wounds drives fibroblasts into a state of high mechanical tension, leading to the delay of wound healing, exacerbating pathological fibrosis, and even causing tissue dysfunction. Here, an innovative skin stress-shielding hydrogel wound dressing is reported that makes the wound sites shrink as a response to body temperature and then remolds the stress micro-environment of wound sites to reduce the formation of skin scars. Composed of a modified natural temperature-sensitive polymer cross-linked with polyacrylic acid networks, this hydrogel wound dressing has demonstrated a substantial decrease in scar area for full-thickness wounds in rat models. The physical forces exerted by the wound dressing are instrumental in attenuating the activation and transduction of fibroblasts within the wound sites, thereby mitigating the excessive deposition of the extracellular matrix (ECM). Notably, the wound dressing significantly down-regulates the expression of transforming growth factor-β1(TGF-β1) and collagen I, while concurrently exerting a dramatic inhibitory effect on the integrin-focal adhesion kinase (FAK)/phosphorylated-FAK (p-FAK) signaling pathway. Collectively, the fabrication of functional hydrogels with a stress-shielding profile is a new route for achieving scar-less wound healing, thus offering immense potential for improving clinical outcomes and restoring tissue integrity.

摘要

伤口周围的应力集中会使成纤维细胞处于高机械张力状态,导致伤口愈合延迟,病理性纤维化加剧,甚至导致组织功能障碍。在这里,报道了一种创新的皮肤应力屏蔽水凝胶伤口敷料,它可以使伤口部位随着体温收缩,然后重塑伤口部位的应力微环境,减少皮肤疤痕的形成。这种水凝胶伤口敷料由经过改性的天然温敏聚合物与聚丙烯酸网络交联而成,在大鼠全层伤口模型中,显著减少了疤痕面积。伤口敷料施加的物理力有助于减弱伤口部位成纤维细胞的激活和转导,从而减轻细胞外基质(ECM)的过度沉积。值得注意的是,该伤口敷料显著下调转化生长因子-β1(TGF-β1)和胶原蛋白 I 的表达,同时对整合素-粘着斑激酶(FAK)/磷酸化粘着斑激酶(p-FAK)信号通路产生强烈的抑制作用。总之,具有应力屏蔽特性的功能性水凝胶的制备为实现无疤痕伤口愈合提供了新途径,从而为改善临床结果和恢复组织完整性提供了巨大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/1ccfb456bc6a/ADVS-11-2306018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/4713217f644f/ADVS-11-2306018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/dd12a3ce1427/ADVS-11-2306018-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/d75320d0e594/ADVS-11-2306018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/41fb227948f0/ADVS-11-2306018-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/ba68e5c3a28e/ADVS-11-2306018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/1ccfb456bc6a/ADVS-11-2306018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/4713217f644f/ADVS-11-2306018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/dd12a3ce1427/ADVS-11-2306018-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/d75320d0e594/ADVS-11-2306018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/41fb227948f0/ADVS-11-2306018-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/ba68e5c3a28e/ADVS-11-2306018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8468/11538717/1ccfb456bc6a/ADVS-11-2306018-g002.jpg

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