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It has been shown that upregulated MMPs in activated astrocytes in the ONH degrade the extracellular matrix (ECM) after retinal I/R injury in mice.[53] As a consequence the ECM is remodeled and degeneration of the lamina cribrosa occurs, which predisposes the RGCs towards compression[54, 55] and can cause further vascular dysregulation.[56] Indeed, we previously showed that the thickness of the lamina cribrosa, which indicates its degeneration, was related to BF in the ONH in glaucoma.[57] Astrocytes also release endothelin, which acts as a strong inducer of vasoconstriction[50] and prevents axonal transportation in the RGCs.[58] Furthermore, although NO in the astrocytes does not itself damage RGCs, it can be converted into the form of peroxynitrite (ONOO - )