Gliosis and Innate Inflammation in Glaucoma
Neuroinflammation is a key mediator of cell death in neurodegenerative diseases of the retina and brain. Our work showed that astrogliosis is toxic to retinal ganglion cells in a mouse model of glaucoma. We are currently pursuing both basic and translational projects studying the role resident microglia and infiltrating macrophages play in the death of retinal ganglion cells.
Check out our poster at ARVO 2024!
Dr. Cui’s talk at ARVO 2024 Bench to Bedside: Clinical Trial Design, Outcomes Assessment, and Regulatory Approval in Gene Therapy
The lab will be at ARVO 2025 (Salt Lake City):
Paper Session: “Hot Topics in Glaucoma”
May 5, 2025 from 3:00 PM to 4:45 PM
Minisymposium: “Charting the course from bench to bedside: Lessons learned, common pitfalls, and regulatory approval in ophthalmic drug and device development”
May 6, 2025 from 3:30 PM to 5:15 PM
Iron Chelation in Glaucoma
Although iron plays a crucial role in cellular metabolism, in excess it is a generator of oxidative stress. Oxidative stress has long been implicated in glaucoma pathogenesis. In close collaboration with the Dunaief lab, we are evaluating iron chelation as a neuroprotective mechanism in glaucoma.
Mitochondrial Dysfunction and Glaucoma
Retinal ganglion cells and the optic nerve are susceptible to mitochondrial dysfunction, which results in increased oxidative stress and impaired ATP synthesis. In collaboration with the Wallace lab, we are evaluating the ocular phenotype in both mouse and humans with mitochondrial DNA mutations affecting the electron transport chain. Our study tests for a direct connection between genetically-determined mitochondrial dysfunction and glaucoma.