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瘢痕与挛缩:生物学原理

Scar and contracture: biological principles.

作者信息

Kwan Peter, Hori Keijiro, Ding Jie, Tredget Edward E

机构信息

Division of Plastic and Reconstructive Surgery, Department of Surgery, 2D2.28 WMC, University of Alberta, 8440-112 Street, Edmonton, AB T6G 2B7, Canada.

出版信息

Hand Clin. 2009 Nov;25(4):511-28. doi: 10.1016/j.hcl.2009.06.007.

DOI:10.1016/j.hcl.2009.06.007
PMID:19801124
Abstract

Dysregulated wound healing and pathologic fibrosis cause abnormal scarring, leading to poor functional and aesthetic results in hand burns. Understanding the underlying biologic mechanisms involved allows the hand surgeon to better address these issues, and suggests new avenues of research to improve patient outcomes. In this article, the authors review the biology of scar and contracture by focusing on potential causes of abnormal wound healing, including depth of injury, cytokines, cells, the immune system, and extracellular matrix, and explore therapeutic measures designed to target the various biologic causes of poor scar.

摘要

伤口愈合失调和病理性纤维化会导致异常瘢痕形成,从而在手烧伤后产生不良的功能和美学效果。了解其中潜在的生物学机制有助于手外科医生更好地应对这些问题,并为改善患者预后指明新的研究方向。在本文中,作者通过聚焦异常伤口愈合的潜在原因,包括损伤深度、细胞因子、细胞、免疫系统和细胞外基质,来综述瘢痕和挛缩的生物学机制,并探讨针对导致不良瘢痕形成的各种生物学原因的治疗措施。

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1
Scar and contracture: biological principles.瘢痕与挛缩:生物学原理
Hand Clin. 2009 Nov;25(4):511-28. doi: 10.1016/j.hcl.2009.06.007.
2
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A Rodent Model of Hypertrophic Scarring: Splinting of Rat Wounds.一种增生性瘢痕的啮齿动物模型:大鼠伤口的夹板固定。
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MicroRNA‑486‑5p inhibits the growth of human hypertrophic scar fibroblasts by regulating Smad2 expression.微小 RNA-486-5p 通过调控 Smad2 表达抑制人增生性瘢痕成纤维细胞的生长。
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