PURPOSE 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. METHODS Literature review. RESULTS 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. CONCLUSIONS 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.].

中文翻译：

---

上皮基底膜和Descemet基底膜对角膜瘢痕形成的协调调节。

目的概述上皮基底膜（EBM）和Descemet基底膜（DBM）在调节角膜损伤，感染，手术和角膜疾病后瘢痕形成（纤维化）中的协调作用的重要性。方法文献综述。结果尽管存在分子和超微结构差异，但EBM和DBM协同作用，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的进入基质，其中这些调节剂的持续水平会触发成纤维细胞的发育和持久性，而成纤维细胞会产生通常不存在于角膜基质中的紊乱，不透明的细胞外基质。这些成肌纤维细胞及其产生的细胞外基质的发育通常对穿透性角膜移植术，LASIK扣眼皮瓣，持续性上皮缺损，微生物性角膜炎，Descemet剥离自动内皮角膜移植术或Desmet膜内皮内皮角膜移植术后角膜的视觉功能有害，在其他情况下，例如LASIK皮瓣的疤痕边缘和穿透性角膜移植术中的供体-受体界面。努力调节EBM和DBM的修复或替代，从而调节成肌纤维细胞的发育或消失，应该是屈光和角膜手术，感染，外伤或角膜疾病提供的治疗的主要重点。结论EBM和DBM是促纤维化生长因子定位的关键调节剂，例如TGF-β，可调节产生角膜疤痕（基质纤维化）的成纤维细胞的发育和持久性。再生或修复EBM和/或DBM并干扰成肌纤维细胞发育或促进其消失的治疗工作通常是临床结果的关键。[J Refract Surg。2019; 35（8）：506-516。]。