The mechanism and targeted therapy of zinc mediating retinal ganglion cell injury through histone H4 deacetylation
Objective: Mammalian optic nerve cannot regenerate once injured. Our previous study found that mobile zinc (Zn2+) increased rapidly after optic nerve injury and it comes from amacrine cell (AC). Whether chelating Zn2+ or specifically knocked out zinc transporter 3 (ZnT3) in ACs significantly [for full text, please go to the a.m. URL]
Institutions
- Sun Yat-sen University (CN)
Publication Details
- Journal
- German Medical Science (German Research Foundation)
- Published
- 2025-05-09
- DOI
- https://doi.org/10.3205/24artvis09
- Primary Topic
- Spam and Phishing Detection
- Type
- article
- Field-Weighted Citation Impact
- 0.00