Iridocorneal endothelial syndrome manifesting 4.5 years after toric implantable collamer lens implantation: a case report.

Age-related macular degeneration (AMD) is a leading cause of irreversible central vision loss in older adults worldwide [, ]. Clinically, AMD is characterized by progressive dysfunction and degeneration of the retinal pigment epithelium (RPE), photoreceptors, and adjacent outer retina in the macular region. Advanced AMD is broadly classified into geographic atrophy (GA) and neovascular AMD (nAMD), marked by choroidal neovascularization and exudative lesions []. Although intravitreal anti–vascular endothelial growth factor (anti-VEGF) therapy has substantially improved the management of nAMD, therapeutic response varies considerably among patients, and a meaningful proportion of eyes show suboptimal anatomical and/or functional improvement after the loading phase []. Therefore, clinically accessible biomarkers that may assist in AMD detection and help stratify treatment response in nAMD remain of considerable interest. AMD is a multifactorial age-related retinal disorder involving aging, oxidative stress, mitochondrial dysfunction, chronic inflammation, and dysregulation of complement activation [–]. Among these mechanisms, oxidative stress–induced RPE injury is considered a central pathogenic event, as it promotes cellular senescence, mitochondrial damage, and impaired retinal homeostasis. Increasing evidence indicates that microRNAs (miRNAs) participate in these stress-related processes and may represent both mechanistic mediators and clinically informative circulating molecules in AMD [–]. MicroRNA-34a (miR-34a) is a well-recognized regulator of aging, oxidative stress, and apoptosis. In our previous studies, we showed that miR-34a is involved in oxidative stress–related premature senescence in RPE cells and that suppression of miR-34a alleviates oxidative injury []. We further demonstrated that miR-34a directly targets SIRT1 and activates the p66Shc pathway, thereby reducing the tolerance of senescent RPE cells to oxidative stress []. These findings support a mechanistic link between miR-34a and key pathogenic events relevant to AMD.