Integrated tear proteomics define the molecular blueprint of corneal epithelial repair

TL;DR

This study identifies a shared tear protein signature across species that reflects corneal healing, offering a practical tool for monitoring eye recovery and guiding treatments.

Contribution

The study introduces a conserved tear proteomic panel that stages corneal injury and healing in both humans and mice.

Findings

A third of the injury response is shared between species, focusing on immune activation and tissue repair.

A tear biomarker panel including transferrin, hemopexin, albumin, and others tracks injury and healing dynamics.

Standardized sampling at D0/D3 can assess damage and healing, aiding clinical decisions and drug testing.

Abstract

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.