Enhanced Retinal Ganglion Cell Survival via Autophagy Activation in a Novel Retinal Ischemia/Reperfusion Rat Model
Si Hyung Lee, Jung Woo Han, Su-ah Yoon, Hun Soo Chang, Tae Kwann Park
TL;DR
This study shows that activating autophagy before retinal injury can protect retinal ganglion cells, offering a potential new treatment for glaucoma.
Contribution
A novel rat model of retinal ischemia/reperfusion was developed, revealing that pre-injury autophagy activation protects retinal ganglion cells.
Findings
A rat model using double circumlimbal sutures reliably induces retinal ischemia/reperfusion injury.
Pre-injury rapamycin treatment significantly enhances retinal ganglion cell survival via autophagy activation.
Autophagy markers peak early after reperfusion but decline by 48 hours, while mTOR pathway components show an inverse pattern.
Abstract
Autophagy is a fundamental catabolic process that degrades and recycles intracellular components, serving as a key survival mechanism in neurons. In glaucomatous optic neuropathy, autophagy has been linked to both protection of retinal ganglion cells (RGCs) and their accelerated loss, yet its precise impact remains unresolved. In this study, we established and validated a straightforward rat model of retinal ischemia/reperfusion (I/R) using double circumlimbal sutures, which reliably produced RGC apoptosis, retinal thinning, and axonal degeneration compared with controls. Early after reperfusion (1–6 h), robust induction of the autophagy marker LC3B was observed, but this activation diminished within 48 h. Other autophagy-related proteins, including ATG4, ATG7, Beclin-1, and p62, followed similar temporal patterns, while components of the mammalian target of rapamycin (mTOR) pathway…
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Taxonomy
TopicsAutophagy in Disease and Therapy · Glaucoma and retinal disorders · Retinal Diseases and Treatments