With the large number of internal eye surgeries, damage to the corneal endothelium is gradually increasing, but further exploration of the factors affecting endothelial repair will become a topic in ophthalmology because of the non-regenerative nature of corneal endothelial cells, which poses many difficulties for clinical treatment. It has been shown that transfer growth factor β2 (TGF-β2) is present in large amounts in atrial fluid, which upregulates the expression of p27kip1 (a cell cycle protein-dependent kinase inhibitor) in corneal endothelial cells, and the expression of p27kip1 inhibits the division of corneal endothelial cells, so TGF-β2 plays an inhibitory role in the proliferation of corneal endothelial cells for repair. smad is a new protein family, and corneal endothelial cells can express Smad2, 3, 4, and 7. This experiment used Smad7 to block the intracellular signaling of TGF-β2, thus antagonizing the inhibitory effect of TGF-β2 on corneal endothelial cell proliferation and achieving the purpose of accelerating corneal endothelial damage repair. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) and Western blotting were used to determine the expression of Smad in corneal endothelial cells; [3H]-labeled thymidine uptake assay was used to evaluate the inhibitory effect of TGF-β2 on DNA replication in corneal endothelial cells; rabbit corneal endothelial cells were transfected with adenovirus carrying murine Smad7 cDNA (AdCMV- Smad7). Endothelial cells were transfected with adenovirus carrying murine LacZ cDNA (AdCMV-LacZ) as a control, and the inhibitory effect of Smad7 on TGF-β2 was determined by immunoblot hybridization; rabbit corneal endothelial cells expressing Smad7 were cultured in vitro, and the endothelial repair process was observed under the condition of mechanical damage to endothelial cells. Results: 1. In vitro cultured rabbit corneal endothelial cells expressed Smad7; 2. TGF-β2 significantly inhibited DNA replication in rabbit corneal endothelial cells; 3. Overexpressed Smad7 eliminated the anti-proliferative effect of exogenous TGF-β2 on endothelial cells, but LacZ did not; 4. Transfection of adenovirus carrying Smad7 into rabbit corneal endothelial cells accelerated corneal endothelial injury repair. Conclusion: Overexpression of Smad7 can inhibit the anti-proliferative effect of TGF-β2, and by changing the expression of Smad7 in corneal endothelial cells, the purpose of healing corneal endothelial injury can be achieved. The repair of corneal endothelial injury in vitro includes both proliferation and migration of endothelial cells, and the migration process of corneal endothelial cells expressing Smad7 precedes the proliferation process, and the overexpression of Smad7 mainly affects the migration process of endothelial cells. The authors concluded that altering Smad7 expression in corneal endothelial cells may have some clinical therapeutic promise for endothelial cell repair.