Corneal fibrosis develops in response to injury, infection, postsurgical complications, or underlying systemic disease that disrupts the homeostasis of the tissue leading to irregular extracellular matrix deposition within the stroma. The mechanisms that regulate corneal scarring are focused heavily on the canonical transforming growth factor-β pathway and relevant activators, and their role in promoting myofibroblast differentiation. In this paper, we discuss the biochemical pathways involved in corneal fibrosis in the context of different injury models-epithelial debridement, superficial keratectomy, and penetrating incision. We elaborate on the interplay of the major pro-fibrotic factors involved in corneal scar development (e.g., transforming growth factor-β1, thrombospondin-1, and ανβ6), and explore a novel role for extracellular vesicles secreted by the wounded epithelium and the importance of the basement membrane.
摘要: 角膜纤维化继发于外伤、感染、术后并发症或潜在的系统性疾病, 这些疾病会破环组织的内环境稳态, 导致基质中不规则的细胞外基质沉积。调控角膜瘢痕形成的机制主要集中在经典的转化生长因子-β通路和相关的激活因子, 以及它们在促进肌成纤维细胞分化中的作用。本文从不同的损伤模型——上皮清创术、浅表角膜切除术和穿透性切口模型, 探讨了角膜纤维化的生物化学信号通路。我们阐述了角膜瘢痕形成过程中主要的促纤维化因子 (如转化生长因子-β1、血小板反应蛋白-1和ανβ6) 的相互作用, 并探讨了损伤上皮细胞分泌的细胞外囊泡的新作用和基底膜的重要性。.