Corneal Surface Response And Refractive Stability After Lasik: Integrating Tear Microrna Signatures And Epithelial Remodeling

To assess corneal-surface recovery and refractive stability after LASIK by integrating tear microRNAs, TGF-β2, and epithelial remodeling.

Clinical study (Ukraine)

The prospective cohort included 150 eyes (150 patients) undergoing myopic LASIK. Preoperative tear miR-146a-5p, miR-450b-5p, and TGF-β2 were measured. Postoperatively, dry eye disease (DED), epithelial thickness change (ΔCET; anterior segment OCT), and Corneal Irregularity Measurement (CIM;Placido-disk topography), were evaluated. Refractive regression was defined as a myopic shift >0.50 D at 12 months versus 3 months. Eyes were assigned to three rule-based profiles (A–C). Non-parametric and categorical tests were performed. Linear associations were evaluated using Pearson correlation, and multivariable linear regression identified independent predictors of refractive change. Principal component analysis (PCA) was applied for visualization.

PCA showed clear separation of the three profiles. Regression risk was 4.3% in Profile A, 55.6% in Profile B (RR 12.92; 95% CI 4.55–36.69), and 12.8% in Profile C. Biomarker patterns differed: Profile B showed lower miR-146a-5p, higher miR-450b-5p, and reduced TGF-β2; Profile A showed the opposite, and Profile C was intermediate. Threshold gradients were marked (miR-146a-5p ≤0.85: 8.6% vs 61.1%; miR-450b-5p >1.95: 7.5% vs 50%; TGF-β2 <1755 pg/mL: 9.7% vs 72.2%). Correlations supported a cascade: miR-450b-5p–TGF-β2 (r=−0.80), TGF-β2–ΔCET (r=−0.75), ΔCET–refractive change (r=−0.73). In multivariable regression (adjusted R²=0.553), ΔCET was the strongest independent predictor (p<0.001); TGF-β2 remained independently associated (p=0.003).

Post-LASIK refractive stability is primarily driven by epithelial remodeling (ΔCET), linking tear biomarker patterns, ocular-surface status, and optical outcome within an integrated biological–morphological pathway. Tear microRNAs and TGF-β2 act as upstream regulators within an integrated biological–morphological pathway rather than as isolated predictors.