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职业迁徙
个人简介
Description of Research Expertise
Research Interests:
Understanding glaucoma pathogenesis and identifying effective treatments for a blinding disease.
Keywords:
ophthalmology; glaucoma; neuroprotection; neurodegeneration; GLP-1 receptor agonists; iron chelation; mitochondria; retinal ganglion cells; optic nerve; intraocular pressure
Research Description:
Glaucoma is characterized by loss of retinal ganglion cells leading to permanent vision loss. It is the leading cause of irreversible blindness and is projected to affect 112 million people worldwide by 2040. Elevated intraocular pressure is a well-known risk factor for disease onset and progression, and intraocular pressure reduction is the only therapeutic mechanism available to slow disease progression. Because glaucoma can continue to progress in a significant number of patients despite intraocular pressure normalization, new therapies are urgently needed to prevent vision loss in patients suffering from glaucoma.
My lab seeks to elucidate the pathogenic mechanisms contributing to glaucoma and identify new and innovative therapies for glaucoma. My lab is actively evaluating GLP-1 receptors agonists as neuroprotective agents in glaucoma (Sterling et al. Cell Reports. 2020; Sterling et al. Br J Ophthalmol. 2021). In collaboration with the lab of Joshua Dunaief, we also demonstrated that iron chelation rescues retinal ganglion cells and promotes optic nerve axon survival following intraocular pressure elevation. Finally, we are characterizing a mouse with inherited deficits affecting the mitochondrial electron transport chain resulting in retinal ganglion cell loss as a model for normal tension glaucoma.
Research Interests:
Understanding glaucoma pathogenesis and identifying effective treatments for a blinding disease.
Keywords:
ophthalmology; glaucoma; neuroprotection; neurodegeneration; GLP-1 receptor agonists; iron chelation; mitochondria; retinal ganglion cells; optic nerve; intraocular pressure
Research Description:
Glaucoma is characterized by loss of retinal ganglion cells leading to permanent vision loss. It is the leading cause of irreversible blindness and is projected to affect 112 million people worldwide by 2040. Elevated intraocular pressure is a well-known risk factor for disease onset and progression, and intraocular pressure reduction is the only therapeutic mechanism available to slow disease progression. Because glaucoma can continue to progress in a significant number of patients despite intraocular pressure normalization, new therapies are urgently needed to prevent vision loss in patients suffering from glaucoma.
My lab seeks to elucidate the pathogenic mechanisms contributing to glaucoma and identify new and innovative therapies for glaucoma. My lab is actively evaluating GLP-1 receptors agonists as neuroprotective agents in glaucoma (Sterling et al. Cell Reports. 2020; Sterling et al. Br J Ophthalmol. 2021). In collaboration with the lab of Joshua Dunaief, we also demonstrated that iron chelation rescues retinal ganglion cells and promotes optic nerve axon survival following intraocular pressure elevation. Finally, we are characterizing a mouse with inherited deficits affecting the mitochondrial electron transport chain resulting in retinal ganglion cell loss as a model for normal tension glaucoma.
研究兴趣
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CELLno. 2 (2024): 464-480.e10
medRxiv : the preprint server for health sciences (2024)
Advances in Ophthalmology and Optometry (2024)
BMJ OPEN OPHTHALMOLOGYno. 1 (2023)
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeuticsno. 3 (2023): 896-907
American Journal of Ophthalmology Case Reports (2023): 101786-101786
Frontiers in cellular neuroscience (2023): 1156829-1156829
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