人角膜基质细胞(HCSCs)是一类呈静息状态的神经嵴间充质细胞,是负责分泌基质的高度特化的透明组织,在维持角膜透明度和人眼正常视觉功能等方面发挥重要作用。正常情况下,角膜基质细胞呈静息状态并表现为扁平、树突状,在角膜受到创伤刺激后被激活,激活状态的人角膜基质细胞(HCK)向修复表型转变,发生凋亡或向角膜成纤维细胞表型和肌成纤维细胞表型转化。HCSCs的表型转化与人角膜损伤修复过程所引起的瘢痕组织形成以及角膜透明度降低等方面具有密切关系。本文通过对HCSCs的3种表型、表型标志物、表型间转化以及体外转化的机制进行综述,发现通过干预HCK向纤维化表型转化过程及TGF-β/Smad等相关信号通路可以抑制角膜纤维化。因此,深入研究HCSCs表型转化的分子机制及干预角膜瘢痕形成的调控机制,有助于临床防治患者角膜纤维化和角膜术后混浊。
Human corneal stromal cells (HCSCs), a type of resting neural crest mesenchymal cell, are highly specialized transparent tissues responsible for the secretion of stroma and play an important role in maintaining the transparency of the cornea and the normal visual function of human eye.Normally, corneal stromal cells are quiescent, flat and dendritic.After the cornea is stimulated by trauma, the corneal stromal cells will be activated, and the activated human corneal keratocytes (HCK) will turn to a repair phenotype, undergo apoptosis or transform to corneal fibroblast phenotype and myofibroblast phenotype.The phenotype transformation of HCSCs is closely related to the formation of scar tissue and the reduction of ocular transparency caused by the repair process of human corneal injury.In this article, three phenotypes, phenotypic markers, phenotype transformation and in vitro transformation mechanisms of HCSCs were reviewed, and it was found that corneal fibrosis could be inhibited by interfering with the transformation process of HCK to fibrotic phenotype and TGF-β/Smad signaling pathways.Therefore, in-depth study of the molecular mechanism of phenotypic transformation of HCSCs and the regulatory mechanism of intervention in corneal scarring formation is helpful for prevention and treatment of corneal fibrosis and postoperative corneal opacity in patients.
杨怡,牛阳,袁玲. 人角膜基质细胞的表型研究进展[J]. 中华实验眼科杂志,2022,40(09):874-879.
DOI:10.3760/cma.j.cn115989-20200626-00455版权归中华医学会所有。
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