Regulated cell death in age-related macular degeneration: Regulatory mechanisms and therapeutic potential

Age-related macular degeneration (AMD) represents a predominant cause of blindness among older adults, with limited therapeutic options currently available. Oxidative stress, inflammation, and retinal pigment epithelium injury are recognized as key contributors to the pathogenesis of AMD. Regulated cell death plays a pivotal role in mediating cellular responses to stress, maintaining tissue homeostasis, and contributing to disease progression. Recent research has elucidated several regulated cell death pathways—such as apoptosis, ferroptosis, pyroptosis, necroptosis, and autophagy—that may contribute to the progression of AMD owing to cell death in the retinal pigment epithelium. These discoveries open new avenues for therapeutic interventions in patients with AMD. In this review, we provide a comprehensive summary and analysis of the latest advancements regarding the relationship between regulated cell death and AMD. Moreover, we examined the therapeutic potential of targeting regulated cell death pathways for the treatment and prevention of AMD, highlighting their roles as promising targets for future therapeutic strategies. • Age-related macular degeneration (AMD) has currently limited therapeutic options. • So far, the role of regulated cell death in AMD pathology has been neglected. • Apoptosis, ferroptosis, pyroptosis, necroptosis, and autophagy contribute to AMD. • Key elements in their pathways are promising therapeutic targets in AMD.