Mitochondria are vital organelles that support numerous cellular functions, including ATP production, regulation of apoptosis, calcium homeostasis, and antiviral defense. To maintain these functions, mitochondria undergo continuous remodeling through membrane fusion, fission, selective clearance (mitophagy), and biogenesis. Our lab develops advanced fluorescent reporter mouse models to study the dynamic behavior of the mitochondrial network in ocular and neural tissues. These models allow for high-resolution, cell-specific imaging of mitochondrial recycling, membrane dynamics, and interactions across various cell types. By applying these tools in models of glaucoma and inherited mitochondrial optic neuropathy, we can examine how disruptions in mitochondrial dynamics contribute to disease progression and identify potential avenues for therapeutic intervention.

Glaucoma is the leading cause of irreversible blindness worldwide, affecting over 80 million people. A key site of dysfunction in glaucoma is the trabecular meshwork (TM), a porous tissue responsible for draining aqueous fluid from the eye. When this drainage is impaired, intraocular pressure increases—a major risk factor for vision loss. Our lab investigates how mitochondrial health in the TM contributes to the development and progression of glaucoma. We analyze mitochondrial DNA from TM tissue collected during glaucoma and corneal surgeries to identify genetic variants associated with ocular hypertension and disease susceptibility. Using TM cell from donor tissue, we model disease processes using primary cell cultures and anterior segment perfusion. By integrating cutting-edge cell biology, genomic analysis, and multi-omic profiling, we aim to uncover how mitochondrial dysfunction affects TM biology and identify new therapeutic targets. While current treatments focus on lowering IOP, our long-term vision is to develop strategies that restore or preserve mitochondrial function as a novel approach to glaucoma therapy.

Mitochondria are unique organelles that contain their own genome—a 16.6 kb circular DNA molecule encoding essential subunits of the electron transport chain. Mutations in mitochondrial DNA (mtDNA) lead to severe ocular and metabolic disorders, often manifesting in infancy or early childhood, for which no curative treatments currently exist. Our laboratory is developing a CRISPR-based platform to target mtDNA mutations with the goal of rescuing these disease phenotypes. We have identified both gene-encoded and synthetic approaches for delivering CRISPR guide RNAs into mitochondria, a critical step toward enabling mitochondrial genome editing. This technology is currently being validated in cellular and tissue models of mtDNA-associated diseases.

As a board-certified glaucoma specialist, I am particularly interested in clinical research that evaluates patient outcomes following therapeutic interventions and the implementation of novel screening technologies. Our team has recently developed a translational mouse model to study the efficacy and complications of transscleral cyclophotocoagulation, a commonly used laser treatment for glaucoma. In parallel, we have identified a small case series of patients who experienced corneal complications following this procedure. Several ongoing projects in our lab aim to investigate how various glaucoma treatments impact corneal health and nerve innervation. By translating clinical observations into targeted research questions, our laboratory leverages interdisciplinary methodologies—including molecular and cell biology, bioinformatics, and data science—to advance understanding and improve patient care in glaucoma.