STAT蛋白
细胞外基质
增生性瘢痕
细胞生物学
体内
激活剂(遗传学)
下调和上调
化学
癌症研究
医学
生物
伤口愈合
信号转导
病理
外科
内科学
车站3
生物化学
受体
基因
生物技术
作者
Qingde Zhou,Jianxiang Gong,Jianing Bi,Xuanxin Yang,Chen Lü,Lijia Li,Min Chen,Jianqiu Cai,Rongshuai Yang,Xiaokun Li,Zhiming Li,Xiaojie Wang
标识
DOI:10.1016/j.jid.2021.12.018
摘要
Hypertrophic scar is a common complication of burns, skin trauma, and postoperative trauma, which involves excessive proliferation of fibroblasts and accumulation of a large amount of disorganized collagen fibers and extracellular matrix. KGF-2 plays important roles in the regulation of cellular homeostasis and wound healing. In this study, we investigated the effect and underlying mechanism of KGF-2 on scar formation after wound healing both in vitro and in vivo. We show that KGF-2 attenuates mechanical stress-induced scar formation while promoting wound healing. Mechanistically, KGF-2 inhibits STAP-2 expression and signal transducer and activator of transcription 3 activation, leading to significantly reduced collagen I and collagen III levels. Our results provide an insight into the role of KGF-2 in wound healing and scar formation and the therapeutic potential for reducing scarring while promoting wound healing.
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