Figure 10.
Silencing of S100A4 downregulated the PI3K/Akt/mTOR pathway, enhanced autophagy, and promoted wound healing of rabbit cornea after alkali burn. After S100A4 silencing, the phosphorylation of the PI3K/Akt/mTOR was decreased significantly. The inhibition of the PI3K/Akt/mTOR pathway promoted the autophagy of rCSCs after alkali burn, led to the differentiation of rCSCs into corneal cells, and inhibited the proliferation, invasion, and migration of rCSCs, thereby promoting the wound healing after alkali burn.