Ferroptosis, a newly identified, iron-dependent type of programmed cell death, is active in several diseases, such as heart disease, brain damage, and cancer. Its main characteristics commonly involve excess iron accumulation, elevated lipid peroxides and reactive oxygen species, and reduced levels of glutathione and glutathione peroxidase 4 levels. The effects of ferroptosis in eye diseases cannot be underestimated, with ferroptosis becoming a research target in ocular disorders and emerging evidence from a series of in vivo and in vitro researches into ferroptosis revealing its role in eye conditions. However, no report provides comprehensive information on the pathophysiology of ferroptosis in eye diseases and its possible treatments. In the current review, we present an up-to-date overview of ferroptosis biology and its involvement in the pathological processes of ocular diseases. Furthermore, we pose several outstanding questions and areas for future research in this topic. We deem ferroptosis-associated cell death a pivotal new field of scientific study in ocular diseases and consider it a new therapeutic target in the treatment of some eye disorders.
Circular RNAs (circRNAs) play important roles in the pathogenesis of age-related cataract (ARC). CircRNA zinc finger protein 292 (circZNF292, hsa_circ_0004058) is downregulated in ARC lens capsules. Here, we focused on its precise roles in oxidative stress underlying the pathogenesis of ARC. CircZNF292, microRNA (miR)-222-3p, and E2F transcription factor 3 (E2F3) were quantified by quantitative real-time polymerase chain reaction or western blot. Cell viability was assessed by the cell counting kit-8 assay. Cell cycle distribution and apoptosis were detected by flow cytometry. The activities of superoxide dismutase, catalase, and malondialdehyde were measured using the corresponding assay kit. Targeted correlations among circZNF292, miR-222-3p, and E2F3 were verified by the dual-luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Our data showed that circZNF292 was downregulated in ARC tissues and H 2 O 2 -treated human lens epithelial B3 (HLE-B3) cells. Increased expression of circZNF292 alleviated H 2 O 2 -induced cell viability suppression, apoptosis promotion, and oxidative stress enhancement. Mechanistically, circZNF292 directly targeted miR-222-3p, and circZNF292 regulated E2F3 expression through miR-222-3p. MiR-222-3p was a functional mediator of circZNF292 in modulating H 2 O 2 -induced injury in HLE-B3 cells. Furthermore, reduced level of miR-222-3p ameliorated H 2 O 2 -induced HLE-B3 cell damage by upregulating E2F3. Our present study demonstrated that increased expression of circZNF292 ameliorated H 2 O 2 -induced injury in HLE-B3 cells at least in part through the miR-222-3p/ E2F3 axis, highlighting a novel insight into the involvement of circRNAs in the pathogenesis of ARC.
Purpose To describe a case of Bilateral Morning Glory Syndrome (MGS) associated with Unilateral Persistent Fetal Vasculature (PFV) in a 3-day old neonate. Observations A 3-day-old neonate was found bilateral retinal abnormalities due to neonatal eye screening. Dilated fundus exam showed bilateral optic disc dysplasia with the persistent hyaloid vessels in right eye at first. With the progress of the disease, optic disc was enlarged with central umbilication which with a similar anomalous radiating peripapillary vascular appearance, the persistent hyaloid vessels in vitreous cavity of right eye gradually disappear, a large amount of exudation can be seen in the posterior pole retina with macular movement in both eyes. Bilateral vitrectomy was performed in this case, then the condition of the neonate's both eyes is stable until 1 year old. Conclusions and Importance This is a rare case that showing the development of MGS and PFV and the relationship between these two diseases. In addition, we completely observed the whole process of the change of the persistent hyaloid vessels in the vitreous cavity of a case of MGS associated with PFV.
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