Strategies Demonstrating Efficacy in Reducing Wound Contraction In Vivo.

Strategies Demonstrating Efficacy in Reducing Wound Contraction In Vivo.
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展示减少体内伤口收缩功效的策略。

DOI:
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发表时间:
2013
影响因子:
4.9
通讯作者:
Y. Martin
Y. Martin
中科院分区:
医学3区
文献类型:
--
作者:
J. R. Sharpe;Y. Martin

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意义 瘢痕形成仍然是一个重要的临床问题。伤口收缩导致瘢痕形成,并由肌成纤维细胞和跨伤口床的收缩力介导。挛缩形成可能对患者的生活质量产生重大影响,特别是在功能和外观受到影响的情况下。 最新进展 新型组织工程基质、基于细胞的疗法和药物疗法已经显示出在体内模型中伤口收缩的显著减少,特别是在早期时间点。这些在许多情况下伴随着肌成纤维细胞数量的减少,并且在一些情况下伴随着血管生成的增加和新真皮结构的改善。 关键问题 没有动物模型可以复制患者伤口愈合的所有方面。因此,应严格评估从体内研究中获得的信息。需要进一步的研究,特别是那些试图阐明新疗法减少收缩的机制的研究,以获得足够的信心进入临床试验。 未来方向 特别是基因敲除小鼠模型的使用,在肌成纤维细胞转化背后的机制和其他参与产生伤口张力的因素的知识方面取得了重大进展。寻求破坏/改变这些途径的药物治疗和组织工程方法对未来的发展和临床实践的转化有很大的希望。
SIGNIFICANCE Scarring continues to present a significant clinical problem. Wound contraction leads to scarring and is mediated by myofibroblasts and contractile forces across the wound bed. Contracture formation can have a significant impact on the quality of life of the patient, particularly where function and appearance are affected. RECENT ADVANCES Novel tissue-engineered matrices, cell-based therapies, and medicinal therapeutics have shown significant reduction in wound contraction in in-vivo models, particularly at early time points. These have been accompanied in many cases by reduced numbers of myofibroblasts, and in some by increased angiogenesis and improved neodermal architecture. CRITICAL ISSUES There are no animal models that replicate all aspects of wound healing as seen in patients. Therefore, information obtained from in vivo studies should be assessed critically. Additional studies, in particular those that seek to elucidate the mechanisms by which novel therapies reduce contraction, are needed to gain sufficient confidence to move into clinical testing. FUTURE DIRECTIONS The use of knockout mouse models in particular has generated significant advances in knowledge of the mechanisms behind myofibroblast conversion and other factors involved in generating tension across the wound. Medicinal therapeutics and tissue-engineering approaches that seek to disrupt/alter these pathways hold much promise for future development and translation to clinical practice.
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