Epigenetic reprogramming for ocular aging and disease: Mechanisms, biomarkers, and the road to the clinic.
Level 5 - mechanism / opinion, no new human data
Narrative review of preclinical mechanisms and therapeutic concepts with no original clinical data.
PubMed 41577329 · doi:10.1016/j.preteyeres.2026.101442
What was done
This narrative review summarizes the molecular mechanisms underlying epigenetic alterations (such as DNA methylation and histone modifications) in post-mitotic retinal neural cells during ocular aging and diseases like glaucoma and age-related macular degeneration (AMD). It evaluates preclinical evidence on partial epigenetic reprogramming strategies, including transient Yamanaka factor expression and chemical cocktails, and discusses translational pathways and safety concerns.
What was found
The abstract reports no quantitative results or specific effect sizes. It describes preclinical findings demonstrating that resetting dysregulated epigenetic landscapes via transient reprogramming can rejuvenate damaged, aged neurons and restore vision in animal models of optic neuropathy.
Why it matters
Unlike fixed genetic mutations, epigenetic marks are potentially reversible. Demonstrating that cellular rejuvenation strategies can restore visual function in preclinical models highlights a novel therapeutic paradigm for currently irreversible blinding eye diseases.
Limits
The paper is a narrative review presenting no new empirical data or systematic search metrics. The discussed therapeutic interventions remain strictly preclinical, with unresolved concerns regarding delivery, safety, and long-term efficacy in human ocular tissues.
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