Karg · Cellular reprogramming 2023 · Controlled animal experimental study · n=?

Sustained Vision Recovery by OSK Gene Therapy in a Mouse Model of Glaucoma.

Cited 31 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Animal experiment without human subjects

PubMed 38060815 · doi:10.1089/cell.2023.0074 · record verified 2026-08-26

What was done

Mice with glaucoma-induced vision damage received gene therapy expressing the transcription factors Oct4, Sox2, and Klf4 (OSK) delivered via a doxycycline-inducible Tet-On adeno-associated virus (AAV) system. The investigators evaluated continuous versus cyclic OSK expression over a year-long period to track therapeutic efficacy, duration of vision recovery after doxycycline withdrawal, and long-term safety (retinal structure and body weight) for up to 21 months.

What was found

Two months of OSK expression fully restored impaired vision in glaucomatous mice, and continuous expression sustained this recovery for 11 months. Following doxycycline withdrawal, viral transcription returned to baseline at 4 weeks; significant visual improvements persisted for 1 month after cessation before gradually waning, though vision remained above pre-treatment baseline. Continuous OSK expression for 21 months caused no adverse effects on retinal architecture or body weight. The abstract reports no numerical values, variance estimates, or sample sizes.

Why it matters

This study demonstrates that partial epigenetic reprogramming via OSK can provide long-lasting functional recovery of vision in an experimental neurodegenerative disease model without apparent long-term oncogenic or structural toxicity.

Limits

The study was conducted exclusively in a mouse model of glaucoma, meaning human translatability and safety remain untested. The abstract omits sample sizes, exact visual performance metrics, statistical variance, and specific control group details.

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