J Refract Surg. 2019 Aug 1;35(8):506-516. doi: 10.3928/1081597X-20190625-02.
To provide an overview of the importance of the coordinated role of the epithelial basement membrane (EBM) and Descemet's basement membrane (DBM) in modulating scarring (fibrosis) in the cornea after injuries, infections, surgeries, and diseases of the cornea.
Literature review.
Despite their molecular and ultrastructural differences, the EBM and DBM act in a coordinated fashion to modulate the entry of transforming growth factor beta (TGF-β) and other growth factors from the epithelium/tear film and aqueous humor, respectively, into the corneal stroma where persistent levels of these modulators trigger the development and persistence of myofibroblasts that produced disordered, opaque extracellular matrix not usually present in the corneal stroma. The development of these myofibroblasts and the extracellular matrix they produce is often detrimental to visual function of the cornea after penetrating keratoplasty, LASIK buttonhole flaps, persistent epithelial defects, microbial keratitis, Descemet stripping automated endothelial keratoplasty, or Descemet membrane endothelial keratoplasty, while being beneficial in other situations such as the scarred edge of LASIK flaps and donor-recipient interface in penetrating keratoplasty. Efforts to modulate the repair or replacement of the EBM and DBM, and thereby the development or disappearance of myofibroblasts, should be a major emphasis of treatments provided by refractive and corneal surgeries, infections, trauma, or diseases of the cornea.
The EBM and DBM are critical modulators of the localization of profibrotic growth factors, such as TGF-β, that modulate the development and persistence of myofibroblasts that produce corneal scars (stromal fibrosis). Therapeutic efforts to regenerate or repair EBM and/or DBM, and interfere with the development of myofibroblasts or facilitate their disappearance are often the key to clinical outcomes. [J Refract Surg. 2019;35(8):506-516.].
概述上皮基底膜 (EBM) 和 Descemet 基底膜 (DBM) 在协调作用中的重要性,以调节角膜损伤、感染、手术和疾病后角膜瘢痕(纤维化)的形成。
文献回顾。
尽管 EBM 和 DBM 在分子和超微结构上存在差异,但它们以协调的方式发挥作用,分别调节转化生长因子-β (TGF-β) 和其他生长因子从上皮/泪膜和房水进入角膜基质,这些调节剂的持续水平触发了肌成纤维细胞的发育和持续存在,肌成纤维细胞产生了通常不存在于角膜基质中的无序、不透明的细胞外基质。这些肌成纤维细胞的发育及其产生的细胞外基质通常对穿透性角膜移植术、LASIK 纽扣孔瓣、持续性上皮缺损、微生物角膜炎、Descemet 剥离自动内皮角膜移植术或 Descemet 膜内皮角膜移植术后的角膜视觉功能有害,但在其他情况下如 LASIK 瓣的瘢痕边缘和穿透性角膜移植术的供体-受体界面有益。调节 EBM 和 DBM 的修复或替代,从而调节肌成纤维细胞的发育或消失,应该是屈光和角膜手术、感染、创伤或角膜疾病所提供治疗的主要重点。
EBM 和 DBM 是调节定位促纤维化生长因子(如 TGF-β)的关键调节剂,这些生长因子调节产生角膜瘢痕(基质纤维化)的肌成纤维细胞的发育和持续存在。再生或修复 EBM 和/或 DBM 并干扰肌成纤维细胞的发育或促进其消失的治疗努力通常是临床结果的关键。[J Refract Surg. 2019;35(8):506-516. ]。