The molecular mechanism of hypertrophic scar

被引:163
作者
Zhu, Zhensen [1 ]
Ding, Jie [1 ]
Shankowsky, Heather A. [1 ]
Tredget, Edward E. [1 ,2 ]
机构
[1] Univ Alberta, Dept Surg, Wound Healing Res Grp, Edmonton, AB T6G 2B7, Canada
[2] Univ Alberta, 2D2-28 WMC,8440-112 St, Edmonton, AB T6G 2B7, Canada
基金
加拿大健康研究院;
关键词
Hypertrophic scar; TGF-beta; Cytokines; Decorin; Matrix metalloproteinases; GROWTH-FACTOR-BETA; LATENT TRANSFORMING GROWTH-FACTOR-BETA-1; MONOCYTE CHEMOATTRACTANT PROTEIN-1; DERMAL FIBROBLASTS CONTRIBUTE; PERIPHERAL-BLOOD FIBROCYTES; MATRIX METALLOPROTEINASE-1; CIRCULATING FIBROCYTES; RECEPTOR CXCR4; DIFFERENTIAL RESPONSES; WOUND CONTRACTION;
D O I
10.1007/s12079-013-0195-5
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Hypertrophic scar (HTS) is a dermal form of fibroproliferative disorder which often develops after thermal or traumatic injury to the deep regions of the skin and is characterized by excessive deposition and alterations in morphology of collagen and other extracellular matrix (ECM) proteins. HTS are cosmetically disfiguring and can cause functional problems that often recur despite surgical attempts to remove or improve the scars. In this review, the roles of various fibrotic and anti-fibrotic molecules are discussed in order to improve our understanding of the molecular mechanism of the pathogenesis of HTS. These molecules include growth factors, cytokines, ECM molecules, and proteolytic enzymes. By exploring the mechanisms of this form of dermal fibrosis, we seek to provide some insight into this form of dermal fibrosis that may allow clinicians to improve treatment and prevention in the future.
引用
收藏
页码:239 / 252
页数:14
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