Targeting Oxidative Stress for Treatment of Glaucoma and Optic Neuritis

Figure 2

The proposed model of the effect of candesartan in EAAC1 KO mice. Increased oxidative stress in EAAC1 KO mice induces the upregulation of AT1-R and TLR4, resulting in increased NO expression via the ASK1 signalling pathway, which leads to RGC death. NO further stimulates AT1-R expression levels through a positive feedback loop. Candesartan blocks AT1-R and exerts neuroprotective effects by suppressing the upregulation of TLR4 and thus reducing ASK1-mediated NO production. This also results in inhibition of the positive feedback loop between NO and AT1-R. Reproduced from Semba et al., [17].