ARB treatment resulted in the suppression of VEGF, ICAM-1, MCP-1, and IL-6, which were upregulated after the induction of corneal neovascularization
(Fig. 6) . These results are compatible with findings in a choroidal neovascularization model of mice.
12 The inhibition of those molecules by ARB may result in the suppression of inflammation and of the angiogenic response in cornea. Among those inflammatory molecules, VEGF is one of the potent stimuli in corneal neovascularization
1 27 and is involved in various angiogenic processes. VEGF promotes endothelial migration, proliferation, and monocyte migration to accelerate vascular permeability and angiogenesis.
27 VEGF also upregulates adhesion molecules such as ICAM-1 through VEGFR2.
27 It has been reported that Ang2 induces in vitro expression of VEGFR2 mRNA.
28 Thus, ARB treatment can efficiently reduce VEGF signaling. In addition to VEGF, other potent angiogenic factors—MCP-1 and IL-6—were also ameliorated by ARB treatment
(Fig. 6) . Furthermore, specific pharmacologic function in telmisartan, unlike other ARB, is a PPAR-γ partial agonist.
20 21 Because PPAR-γ ligand works in an anti-inflammatory role,
20 21 telmisartan may have advantage for reducing inflammation. In fact, one of the PPAR-γ agonists, pioglitazone, inhibited corneal neovascularization in a rat model.
29 Therefore, dramatic inhibition of corneal neovascularization by ARB might be observed in the present study
(Fig. 5) .