Sappington Rebecca M

Joos Karen M, Li Chun, Sappington Rebecca M

This rat study found short, intermittent IOP spikes cause early optic nerve degeneration, including thinning and axon loss, clinically relevant for understanding glaucoma progression.

Sappington Rebecca M, Carlson Brian J, Crish Samuel D, Calkins David J

This study found injecting microbeads into rat/mouse eyes consistently elevated intraocular pressure, causing optic nerve damage. This offers a simple, reliable model for glaucoma research.

Sappington Rebecca M, Sidorova Tatiana, Long Daniel J, Calkins David J

This study found that TRPV1 channels significantly contribute to retinal ganglion cell death and calcium influx under pressure, suggesting TRPV1 antagonism could be a therapeutic target for glaucoma.

Sappington Rebecca M, Calkins David J

Elevated pressure activates retinal microglia via calcium influx, partly dependent on TRPV1, leading to inflammation (IL-6, NFkB). Blocking TRPV1 could reduce glaucoma-related neuroinflammation.

Sappington Rebecca M, Chan Matilda, Calkins David J

Studying glaucoma, researchers found interleukin-6 (IL-6) protects retinal ganglion cells from pressure-induced death. This suggests IL-6 could be a therapeutic target for preserving vision.

Inman Denise M, Sappington Rebecca M, Horner Philip J, Calkins David J

DBA/2 mouse study found elevated IOP correlated with optic nerve axon loss. Surprisingly, corneal thickness strongly predicted axon density, suggesting it could be a glaucoma degeneration index.