Purpose To investigate the changes of the retinal microvascular network and microcirculation in high myopia. Design A cross-sectional, matched, comparative clinical study. Participants Twenty eyes of twenty subjects with non-pathological high myopia (28 ± 5 Years) with a refractive error of −6.31 ± 1.23 Diopters (mean ± standard deviation) and twenty eyes of twenty age- and gender-matched control subjects (30 ± 6 years) with a refractive error of −1.40 ± 1.00 Diopters were recruited. Methods Optical coherence tomography angiography (OCTA) was used to image the retinal microvascular network, which was later quantified by fractal analysis (box counting, Dbox, representing vessel density) in both superficial and deep vascular plexuses. The retinal function imager (RFI) was used to image the retinal microvessel blood flow velocity (BFV). The BFV and microvascular density in the myopia group were corrected for ocular magnification using Bennett’s formula. Results The density of both superficial and deep microvascular plexuses was significantly decreased in the myopia group in comparison to the controls (P < 0.05). The decrease of the microvessel density of the annular zone (0.6 – 2.5 mm), measured as Dbox, was 2.1% and 2.9% in superficial and deep vascular plexuses, respectively. The microvessel density reached a plateau from 0.5 mm to 1.25 mm from the fovea in both groups, but that in myopic group was about 3% lower than the control group. No significant differences were detected between the groups in retinal microvascular BFV in either arterioles or venules (P > 0.05). Microvascular densities in both superficial (r = −0.45, P = 0.047) and deep (r = −0.54, P = 0.01) vascular plexuses were negatively correlated with the axial lengths in the myopic eye. No correlations were observed between BFV and vessel density (P > 0.05). Conclusions Retinal microvascular decrease was observed in the high myopia subjects, whereas the retinal microvessel BFV remained unchanged. The retinal microvascular network alteration may be attributed to ocular elongation that occurs with the progression of myopia. The novel quantitative analyses of the retinal microvasculature may help to characterize the underlying pathophysiology of myopia and enable early detection and prevention of myopic retinopathy.

OCT demonstrated that macular thickness/volume was normally distributed in this sample of Chinese children, with variations in sex and SE. The variables in macular thickness/volume should be considered when diagnosing and monitoring school-aged children with diseases that affect the macula.

Corneal asphericity in this population is related more to corneal quadrant location than to age. The results from this study suggest that degree of myopia and central corneal radius both have a significant though weak association with corneal asphericity in Chinese eyes.

OBJECTIVEMitochondrial reactive oxygen species (ROS) plays a key role in diabetic retinopathy (DR) pathogenesis. However, whether simvastatin decreases diabetes-induced mitochondrial ROS production remains uncertain. The aim of this study was to clarify the beneficial effects and mechanism of action of simvastatin against diabetes-induced retinal vascular damage.RESEARCH DESIGN AND METHODSDiabetic rats and control animals were randomly assigned to receive simvastatin or vehicle for 24 weeks, and bovine retinal capillary endothelial cells (BRECs) were incubated with normal or high glucose with or without simvastatin. Vascular endothelial growth factor (VEGF) and peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α) in the rat retinas or BRECs were examined by Western blotting and real-time RT-PCR, and poly (ADP-ribose) polymerase (PARP), and p38 MAPK were examined by Western blotting. Mitochondrial membrane potential (Δψm) and ROS production were assayed using the potentiometric dye 5,5′,6,6′- Tetrachloro1,1′,3,3′-tetraethyl-benzimidazolylcarbocyanine iodide (JC-1) or CM-H2DCFDA fluorescent probes.RESULTSSimvastatin significantly upregulated PGC-1α (P < 0.01), subsequently decreased Δψm (P < 0.05) and ROS generation (P < 0.01), inhibited PARP activation (P < 0.01), and further reduced VEGF expression (P < 0.01) and p38 MAPK activity (P < 0.01). Those changes were associated with the decrease of retinal vascular permeability, retinal capillary cells apoptosis, and formation of acellular capillaries.CONCLUSIONSSimvastatin decreases diabetes-induced mitochondrial ROS production and exerts protective effects against early retinal vascular damage in diabetic rats in association with the inhibition of mitochondrial ROS/PARP pathway mediated by PGC-1α. The understanding of the mechanisms of action of statins has important implications in the prevention and treatment of mitochondrial oxidative stress-related illness such as DR.

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