Department of Ophthalmology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, Hong Kong, China.
Department of Ophthalmology, University of Pittsburgh Medical Centre, Pittsburgh, Pennsylvania, USA.
Ophthalmic Res. 2021;64(2):178-191. doi: 10.1159/000509030. Epub 2020 May 29.
This review aims to summarise the role of different cells, genes, proteins and lipid in regulating cornea epithelial-stromal homeostasis.
We performed an Entrez PubMed literature search using keywords "human," "cornea," "epithelial," "stromal," "homeostasis," "fibrosis response," and "pathogenesis" on 24th of September 2019, resulting in 35 papers, of which 18 were chosen after filtering for "English language" and "published within 10 years" as well as curation for relevance by the authors.
The 18 selected papers showed that corneal epithelial cells, fibroblasts and telocytes, together with genes such as Klf4, Pax6 and Id found in the cells, play important roles in achieving homeostasis to maintain corneal integrity and transparency. Proteins classified as pro-fibrotic ligands and anti-fibrotic ligands are responsible for regulating cornea stromal fibrosis and extracellular matrix deposition, thus regulators of scar formation during wound healing. Anti-inflammatory ligands and wound repairing ligands are critical in eliciting protective inflammation and promoting epithelial healing, respectively. Protein receptors located on cellular membrane play a role in maintaining intercellular connections as well as corneal hydration.
DISCUSSION/CONCLUSION: These studies prompt development of novel therapeutic strategies such as tear drops or ointments that target certain proteins to maintain corneal homeostasis. However, more in vitro and in vivo studies are required to prove the effectiveness of exogenous administration of molecules in improving healing outcome. Hence, future investigations of the molecular pathways highlighted in this review will reveal novel therapeutic tools such as gene or cell therapy to treat corneal diseases.
本文旨在总结不同细胞、基因、蛋白质和脂质在调节角膜上皮-基质稳态中的作用。
我们于 2019 年 9 月 24 日使用关键词“human”“cornea”“epithelial”“stromal”“homeostasis”“fibrosis response”和“pathogenesis”在 Entrez PubMed 上进行文献检索,共得到 35 篇论文,经过筛选后得到 18 篇与主题相关的英文文献,其中 18 篇论文被认为与主题相关。
这 18 篇论文表明,角膜上皮细胞、成纤维细胞和间质细胞,以及细胞中的 Klf4、Pax6 和 Id 等基因,共同发挥作用以实现稳态,维持角膜的完整性和透明度。归类为促纤维化配体和抗纤维化配体的蛋白质负责调节角膜基质纤维化和细胞外基质沉积,从而调节伤口愈合过程中的瘢痕形成。抗炎配体和伤口修复配体在引发保护性炎症和促进上皮愈合方面分别起着至关重要的作用。位于细胞膜上的蛋白受体在维持细胞间连接和角膜水合作用方面发挥作用。
讨论/结论:这些研究提示人们开发出了新的治疗策略,例如针对特定蛋白质的眼药水或眼药膏,以维持角膜稳态。然而,还需要更多的体外和体内研究来证明外源性给予分子在改善愈合结果方面的有效性。因此,对本文中强调的分子途径进行进一步研究,将揭示出基因或细胞治疗等新型治疗工具,用于治疗角膜疾病。