Tears are easy to collect, repeatable, and reflect the state of the corneal surface—attributes that make them attractive for bedside monitoring after surgery or injury. We performed a cross-species meta-analysis of tear proteomes from patients undergoing photorefractive keratectomy (PRK) and from mice after mechanical epithelial abrasion to define molecular programs that are both conserved and clinically actionable. Roughly one-third of the injury response was shared between species, centering on innate immune activation (complement/acute phase), epithelial migration and cytoskeletal remodeling, and a calibrated suppression of proteolysis. From this overlap we distilled a small, secreted tear panel that stages injury and early resolution in both species: transferrin and hemopexin (iron/heme scavenging), albumin (vascular leak), apolipoprotein A-I (barrier lipid transport), and the coagulation modulators kininogen-1 and α2-antiplasmin (protease/fibrinolysis control). This panel rises at the first post-injury sampling (D0 in humans; 6–12 h in mice) and trends toward baseline during recovery (D3 in humans; ∼24 h in mice), providing a practical kinetic signature for clinical decision-making. Standardized sampling at D0/D3 can therefore quantify acute damage and early healing, enable pharmacodynamic readouts for anti-inflammatory or barrier-stabilizing therapies, and support risk stratification after epithelial procedures. Species-specific differences (human: secretory/immune surveillance; mouse: mitochondrial/metabolic reboot) clarify which preclinical signals are most likely to translate. Together, these findings establish a conserved tear blueprint of corneal repair and nominate a minimal, deployable biomarker set to accelerate clinical monitoring and therapeutic development in ocular surface disease.
Feret et al. (Mon,) studied this question.