The corneal wound healing response is typically initiated by injuries to the epithelium and/or endothelium that may also involve the stroma. However, it can also be triggered by immune or infectious processes that enter the stroma via the limbal blood vessels. For mild injuries or infections, such as epithelial abrasions or mild controlled microbial infections, limited keratocyte apoptosis occurs and the epithelium or endothelium regenerates, the epithelial basement membrane (EBM) and/or Descemet's basement membrane (DBM) is repaired, and keratocyte- or fibrocyte-derived myofibroblast precursors either undergo apoptosis or revert to the parent cell types. For more severe injuries with extensive damage to EBM and/or DBM, delayed regeneration of the basement membranes leads to ongoing penetration of the pro-fibrotic cytokines transforming growth factor (TGF) β1, TGFβ2 and platelet-derived growth factor (PDGF) that drive the development of mature alpha-smooth muscle actin (SMA)+ myofibroblasts that secrete large amounts of disordered extracellular matrix (ECM) components to produce scarring stromal fibrosis. Fibrosis is dynamic with ongoing mitosis and development of SMA + myofibroblasts and continued autocrine-or paracrine interleukin (IL)-1-mediated apoptosis of myofibroblasts and their precursors. Eventual repair of the EBM and/or DBM can lead to at least partial resolution of scarring fibrosis.

角膜伤口愈合反应通常由上皮和/或内皮损伤引发，也可能涉及基质。然而，它也可能由通过角膜缘血管进入基质的免疫或感染过程触发。对于轻度损伤或感染，例如上皮擦伤或轻度控制的微生物感染，会发生有限的角膜细胞凋亡，上皮或内皮再生，上皮基底膜（EBM）和/或后弹力层基底膜（DBM）修复，角膜细胞或内皮细胞再生。纤维细胞衍生的肌成纤维细胞前体要么发生凋亡，要么恢复为亲代细胞类型。对于 EBM 和/或 DBM 广泛损伤的更严重损伤，基底膜再生延迟会导致促纤维化细胞因子转化生长因子 (TGF) β1、TGFβ2 和血小板衍生生长因子 (PDGF) 持续渗透，从而驱动成熟的α-平滑肌肌动蛋白（SMA）+肌成纤维细胞的发育，分泌大量无序的细胞外基质（ECM）成分，产生疤痕基质纤维化。纤维化随着持续的有丝分裂和 SMA + 肌成纤维细胞的发育以及持续的自分泌或旁分泌白细胞介素 (IL)-1 介导的肌成纤维细胞及其前体细胞凋亡而动态变化。 EBM 和/或 DBM 的最终修复可以导致疤痕纤维化至少部分消退。