Jester J V, Petroll W M, Cavanagh H D
Department of Ophthalmology, The University of Texas Southwestern Medical Center at Dallas, 75235-9057, USA.
Prog Retin Eye Res. 1999 May;18(3):311-56. doi: 10.1016/s1350-9462(98)00021-4.
While laser and incisional refractive surgery offer the promise to correct visual refractive errors permanently and predictably, variability and complications continue to hinder wide-spread acceptance. To explain variations, recent studies have focused on the role of corneal wound healing in modulating refractive outcomes. As our understanding of the corneal response to refractive surgery broadens, it has become apparent that the response of one cell, the corneal stromal keratocyte, plays a pivotal role in defining the results of refractive surgery. Studies reviewed herein demonstrate that injury-induced activation and transformation of keratocytes to myofibroblasts control the deposition and organization of extracellular matrix in corneal wounds. Myofibroblasts establish an interconnected meshwork of cells and extracellular matrix that deposits new matrix and contracts wounds using a novel and unexpected "shoe-string-like" mechanism. Transformation of keratocytes to myofibroblasts is induced in culture by transforming growth factor beta (TGFbeta) and blocked in vivo by antibodies to TGFbeta. Overall, myofibroblast appearance in corneal wounds is associated with wound contraction and regression following incisional keratotomy and the development of "haze" or increased scattered light following laser photorefractive keratectomy (PRK). By contrast, absence of myofibroblasts is associated with continued widening of wound gape and progressive corneal flattening after incisional procedures. Based on these studies, we have arrived at the inescapable conclusion that a better understanding of the cellular and molecular biology of this one cell is required if refractive surgery is ever to achieve predictable and safe refractive results.
虽然激光手术和切开性屈光手术有望永久性且可预测地矫正视觉屈光不正，但个体差异和并发症仍然阻碍了其广泛应用。为了解释这些差异，最近的研究聚焦于角膜伤口愈合在调节屈光结果中的作用。随着我们对角膜对屈光手术反应的理解不断深入，越来越明显的是，一种细胞——角膜基质成纤维细胞——的反应在决定屈光手术结果方面起着关键作用。本文综述的研究表明，损伤诱导的成纤维细胞激活和向肌成纤维细胞的转化控制着角膜伤口中细胞外基质的沉积和组织。肌成纤维细胞建立起细胞与细胞外基质的相互连接网络，该网络沉积新的基质，并通过一种新颖且意想不到的“鞋带样”机制使伤口收缩。在培养中，转化生长因子β（TGFβ）可诱导成纤维细胞向肌成纤维细胞转化，而在体内，针对TGFβ的抗体可阻断这种转化。总体而言，角膜伤口中肌成纤维细胞的出现与切开性角膜切开术后伤口收缩和回退以及激光屈光性角膜切削术（PRK）后“雾状混浊”或散射光增加有关。相比之下，没有肌成纤维细胞则与切开手术后伤口裂隙持续增宽和角膜逐渐变平有关。基于这些研究，我们得出了一个不可避免的结论：如果屈光手术想要实现可预测且安全的屈光效果，就需要更好地了解这种细胞的细胞和分子生物学特性。
