Wound healing is one of the most complex biological processes to occur in life. Repair of tissue following injury involves dynamic interactions between multiple cell types, growth factors, inflammatory mediators and components of the extracellular matrix (ECM). Aberrant and uncontrolled wound healing leads to a non-functional mass of fibrotic tissue. In the eye, fibrotic disease disrupts the normally transparent ocular tissues resulting in irreversible loss of vision. A common feature in fibrotic eye disease is the transdifferentiation of cells into myofibroblasts that can occur through a process known as epithelial-mesenchymal transition (EMT). Myofibroblasts rapidly produce excessive amounts of ECM and exert tractional forces across the ECM, resulting in the distortion of tissue architecture. Transforming growth factor-beta (TGFβ) plays a major role in myofibroblast transdifferentiation and has been implicated in numerous fibrotic eye diseases including corneal opacification, pterygium, anterior subcapsular cataract, posterior capsular opacification, proliferative vitreoretinopathy, fibrovascular membrane formation associated with proliferative diabetic retinopathy, submacular fibrosis, glaucoma and orbital fibrosis. This review serves to introduce the pathological functions of the myofibroblast in fibrotic eye disease. We also highlight recent developments in elucidating the multiple signaling pathways involved in fibrogenesis that may be exploited in the development of novel anti-fibrotic therapies to reduce ocular morbidity due to scarring.

伤口愈合是生命中发生的最复杂的生物学过程之一。损伤后的组织修复涉及多种细胞类型，生长因子，炎症介质和细胞外基质（ECM）成分之间的动态相互作用。异常且不受控制的伤口愈合会导致纤维化组织无功能。在眼中，纤维化病会破坏正常透明的眼组织，从而导致不可逆的视力丧失。纤维化性眼病的一个共同特征是细胞转分化为成肌纤维细胞，可以通过称为上皮-间质转化（EMT）的过程发生。肌成纤维细胞迅速产生过量的ECM，并在ECM上施加牵引力，导致组织结构变形。转化生长因子-β（TGFβ）在成肌纤维细胞的分化中起主要作用，并与多种纤维化眼病有关，包括角膜混浊，翼状，肉，前囊膜白内障，后囊膜混浊，增生性玻璃体视网膜病变，与增生性糖尿病性视网膜病相关的纤维血管膜形成黄斑下纤维化，青光眼和眼眶纤维化。这篇综述有助于介绍成纤维细胞在纤维化眼病中的病理功能。我们还强调了阐明纤维化涉及的多种信号通路的最新进展，这些信号通路可用于开发新型抗纤维化疗法以减少因瘢痕形成引起的眼病的发生。