Primary vascular dysregulation and glaucoma

Abstract

The pathogenesis of glaucomatous optic neuropathy is still debated. Ocular blood flow (OBF) in glaucoma patients is generally reduced, particularly in patients with progression of damage in spite of a normal IOP. However, the question of whether this OBF reduction is only secondary to the damage or whether it is a primary causal factor has remained open for a long time. In this review, we try to explain why vascular dysregulation contributes to glaucomatous damage. In people with primary vascular dysregulation, the autoregulation of ocular perfusion is disturbed. Therefore, fluctuations in intraocular pressure (IOP) or blood pressure lead to an unstable oxygen supply. This in turn increases oxidative stress, particularly in the mitochondria of the optic nerve head (ONH). The simultaneous activation of the astrocytes leads to altered gene expression, which contributes to both tissue remodeling in the ONH and the death of retinal ganglion cells. The activated astrocytes produce more metalloproteinase degrading the extracellular matrix. This results in a remodeling of the extracellular matrix, which is basic component of ONH excavation.