缺氧诱导因子-1α在瘢痕疙瘩致病机制中的作用
Role of HIF-1α in pathogenic mechanisms of keloids.
作者信息
Qiu Zi-Kai, Zhang Ming-Zi, Zhang Wen-Chao, Li Zhi-Jin, Si Lou-Bin, Long Xiao, Yu Nan-Ze, Wang Xiao-Jun
机构信息
Department of Plastic and Reconstructive Surgery, Peking Union Medical college Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
出版信息
J Cosmet Dermatol. 2023 May;22(5):1436-1448. doi: 10.1111/jocd.15601. Epub 2023 Jan 31.
BACKGROUDS AND OBJECTIVE
Keloids are defined as overrepairing products that develop after skin lesions. Keloids are characterized by the proliferation of fibroblasts and the overaccumulation of extracellular matrix components (mainly collagen), leading to a locally hypoxic microenvironment. Hence, this article was aimed to review hypoxia in pathogenesis of keloids.
METHODS
We reviewed and summarized the relevant published studies.
RESULTS
Hypoxia results in the accumulation of hypoxia-inducible factor 1α (HIF-1α) in keloids, contributing to overactivation of the fibrotic signaling pathway, epithelial-mesenchymal transition, and changes in metabolism, eventually leading to aggravated fibrosis, infiltrative growth, and radiotherapy resistance.
CONCLUSION
It is, therefore, essential to understand the role of HIF-1α in the pathogenic mechanisms of keloids in order to develop new therapeutic approaches.
背景与目的
瘢痕疙瘩被定义为皮肤损伤后形成的过度修复产物。瘢痕疙瘩的特征是成纤维细胞增殖和细胞外基质成分（主要是胶原蛋白）过度积累，导致局部缺氧微环境。因此，本文旨在综述缺氧在瘢痕疙瘩发病机制中的作用。
方法
我们回顾并总结了相关已发表的研究。
结果
缺氧导致瘢痕疙瘩中缺氧诱导因子1α（HIF-1α）积累，促进纤维化信号通路过度激活、上皮-间质转化和代谢变化，最终导致纤维化加重、浸润性生长和放疗抵抗。
结论
因此，了解HIF-1α在瘢痕疙瘩发病机制中的作用对于开发新的治疗方法至关重要。
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