Faculty


This is an image of Dr. Suchismita Acharya.

Suchismita Acharya, PhD

Assistant Professor

Our current research is focused on expanding the chemical toolbox for neural signaling and anti-inflammation/anti-oxidant pathways to understand the mechanism of action of the disease pathology associated with glaucomatous optic neuropathy, Alzheimer Diseases, Ischemic stroke as well as angiogenesis. Our lab integrates medicinal chemistry, chemical biology, bio-engineering, and drug delivery via nanotechnology. We employ synthetic organic and organometallic chemistry to generate small molecule library for low throughput as well as high throughput screening (target based as well as phenotypic).


This is an image of Dr. Abbot Clark.

Abbot Clark, PhD

FARVO Professor

Abe Clark’s laboratory studies the cell and molecular mechanisms responsible for a variety of eye diseases, especially glaucoma. Glaucoma is a leading cause of irreversible vision loss and blindness in the world. Dr. Clark’s lab has discovered a number of new disease pathways involved in glaucomatous elevation of intraocular pressure. His lab also has identified novel neuroprotective therapies to protect specific retinal neurons, retinal ganglion cells, that are damaged in glaucoma, and also protect the optic nerve and visual centers in the brain. Abe currently mentors 9 graduate students and serves on the editorial board of 4 scientific journals. He has published over 190 peer-reviewed manuscripts and has been invited to present his scientific work at over 110 national and international scientific meetings.


This is an image of Dr. Denise Inman.

Denise Inman, PhD

Associate Professor

My lab investigates the metabolic alterations associated with the pathogenesis of glaucoma. Mitochondria, the organelles responsible for generating energy and coordinating metabolism in the cell, show various signs of dysfunction prior to the degeneration that occurs in glaucoma. Also compromised are the cellular transporters that provide the raw materials for energy generation to the mitochondria. We are establishing ways to limit these changes in order to prevent glaucoma development.


This is an image of Dr. Ankita Jaykumar.

Ankita Jaykumar, PhD

Assistant Professor

My lab investigates the metabolic alterations in the brain associated with the pathogenesis of cognitive dysfunction. Evidence including our recent work highlights the pivotal role of insulin in neuronal functions such as learning and memory. Indeed, dementia is recognized as a neuroendocrine disorder as it is referred to as Type 3 diabetes. Metabolic dysfunction largely due to dysregulation of endocrine signaling, becomes a high-risk factor for memory dysfunction. Although metabolic dysfunction in the brain precedes cognitive dysfunction, how neuronal endocrine signaling regulates brain function is poorly understood. As approximately half of those in the US above the age of 65 are either diabetic or prediabetic, understanding the mechanistic basis of endocrine signaling in the brain is of high urgency with a significant impact on the well-being of our aging society. Our previous work uncovered a molecular mechanism involving ‘WNK Kinases’ as key regulators of neuronal insulin signaling as well as memory. This finding opens a window of opportunity to investigate the mechanism underlying the synergistic relationship between metabolic dysfunction and cognitive disorders.  To advance our understanding of neuronal metabolic regulation, we have developed an interdisciplinary research program that addresses mechanisms of age-based differences in neuroendocrine function and derangements that cause memory decline.


This is an image of Dr. Dimitrios Karamichos.

Dimitrios Karamichos, PhD

Executive Director & Endowed Chair

Lab Mission: Our goal is to discover, develop, and deliver novel therapies for the treatment of corneal trauma and diseases.

The lab is currently running several projects, including the discovery of novel biomarkers and therapeutic solutions for the diagnosis, management, and treatment of corneal fibrosis, keratoconus, and diabetic keratopathy. We have a strong interest in personalized medicine, particularly how factors such as sex, age, and disease severity influence corneal diseases.


This is an image of Dr. Jayoung Kim.

Jayoung Kim, PhD

Assistant Professor

Our lab develops and studies innovative drug delivery systems with the following three major focus areas.

  1. Local drug delivery via 3D-printed, ocular device: We aim to develop polymer-based constructs (contact lens, artificial cornea) with appropriate drug release profiles specific to the applications concerning corneal disease.
  2. Hitchhiking-enabled, organ-specific drug delivery: We aim to develop hollow, polymeric microcapsules that serve as carriers of surface-adsorbed nanoparticles to target specific organs following systemic administration.
  3. Personalized drug delivery to breast tumor: We aim to enhance tumor delivery of a variety of nanoparticle platforms by addressing various phenotypic features that represent interpatient heterogeneity in breast cancer.

This is an image of Dr. Raghu Krishnamoorthy.

Raghu Krishnamoorthy, PhD

Professor, Pharmacology & Neuroscience, North Texas Eye Research Institute

Graduate Faculty Full Member

The major research emphasis is on understanding biochemical and molecular mechanisms underlying the etiology of glaucoma. Specific research interests are to understand the regulation of expression of  the vasoactive active peptides, endothelins, and their receptors, which are thought to contribute to glaucomatous optic neuropathy. The endothelin (ET) system of vasoactive peptides (comprising of ET-1, ET-2 and ET-3) and their G protein coupled receptors (ETA and ETB receptors) have been found to be elevated in animal models of glaucoma. Corroborative findings from several laboratories have demonstrated that ET-1 acting through both vascular and cellular mechanisms produces neurodegenerative effects in glaucoma. ET-1 mediates these effect through activation of the ETA and ETB receptors, leading to optic nerve degeneration and retinal ganglion cell death. Our current projects address the role of endothelins in producing a decline in mitophagy in rodent models of glaucoma. The long-term goals are to develop endothelin receptor antagonists as neuroprotective agents for the treatment for glaucoma.


This is an image of Dr. Xinyue Liu.

Xinyue Liu, PhD

Assistant Professor

My laboratory leverages high-throughput mass spectrometry-based proteomics and quantitative chemoproteomics to systematically characterize disease-relevant cellular mechanisms in blinding ocular disorders, driving the discovery of novel therapeutics. A central focus is Keratoconus (KC), a progressive corneal disease characterized by keratocyte apoptosis, for which no mechanism-based treatments currently exist. We apply advanced cysteine-reactivity profiling to map and prioritize pathogenic and ligandable protein sites—especially those within apoptotic pathways—in primary human corneal fibroblasts. This mechanistic understanding is paired with a covalent drug discovery pipeline, utilizing high-throughput screening of cysteine-reactive chemical libraries to identify small-molecule inhibitors that effectively suppress apoptosis and enhance cell viability, thereby establishing a new paradigm for treating the underlying cellular pathology in KC and other ocular diseases.

This is an image of Dr. Cameron Millar.

Cameron Millar, PhD

Research Assistant Professor

Experienced eye researcher and educator, with both academic and industrial experience, committed to the investigation of ocular anterior segment physiology, aqueous humor dynamics, pharmacology, and glaucoma.  Experienced with in vivo (live animal) and organ perfusion paradigms, as well as small animal research surgical techniques, in the following species: mouse, rat, rabbit, monkey, and bovine.

 


Hongli

Hongli Wu, PhD

Assistant Professor

The central theme of my research is to understand the function of thiol-regulating enzymes and evaluate their therapeutic potential in eye diseases. Of primary interest is the age-related macular degeneration (AMD), the most common retinal disorder that affects 25 million people worldwide, yet its pathogenesis remains poorly understood. The following are our major projects:

Examine how retinal thiol redox dysregulation leads to AMD pathogenesis.
Characterize glutaredoxin 2 (Grx2), a thiol redox-regulating enzyme, knockout mice as a new animal model for AMD.
Identify/screening Grx2 inducers from natural products for AMD treatment.