Rho-Kinase/ROCK as a Potential Drug Target for Vitreoretinal Diseases

Table 1

Comparison between VEGF and Rho/ROCK in disease pathogenesis.

Biological process	VEGF inhibition	Rho/ROCK inhibition
Ischemia	Possible induction of ischemia [24]	Vascular normalization via pericyte coverage [45]; vessel dilation [58]; increased blood velocity and retinal blood flow [59]
Angiogenesis	Antiangiogenesis [81, 82]	Antiendothelial proliferation in vitro [44, 45]; antiendothelial migration in vitro [44, 45]; antiangiogenesis in vivo retina [43, 45]; antiangiogenesis; in vivo choroid [63, 66]
Hyperpermeability	Antipermeability [83, 84]	Antipermeability in choroidal neovascularization [63, 66]
Inflammation	Antileukocyte trafficking [81]; antileukostasis [84]	Antileukostasis [38]; anti-M2 macrophage [63]
Membrane contraction	Possible induction of membrane contraction; and tractional retinal detachment [23]; vessel contraction [25]	Inhibition of membrane contraction in vivo [50, 73]; reduced collagen synthesis in RPE [66]; inhibition of gel; contraction by RPE [72, 73]; anti-RPE proliferation [72]; actin depolymerization in RPE [74]
Neuronal damage	Possible induction of photoreceptor damage [85, 86]	Neuroprotection of RGC [78, 87, 88]
Fibrosis	Risk of inducible fibrosis [22, 65]	Antifibrosis in choroidal neovascularization [66]