North Texas Eye Research Institute Faculty and Staff



Suchismita Acharya, PhDSuchi Updated Headshot (1)

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).

Abbot ClarkAbbot 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.

DoretteDorette Ellis, PhD

Associate Professor

Glaucoma is a disease of the eye that results in blindness. There are two prominent problems in glaucoma. One is high pressure caused by fluid build-up in the front of the eye and the other is loss of structures called retinal ganglion cells in the back of the eye. I am interested in understanding how retinal ganglion cells function and how to help the cells survive in glaucoma. I am also interested in understanding how the fluid in the front of the eye is able to build-up and how to decrease the fluid in glaucoma. Understanding how fluid builds-up and how cells die will allow us to develop therapeutic strategies for the treatment of glaucoma.

DeniseDenise 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.


Nteri DkDimitrios Karamichos, PhD

Executive Director & Endowed Chair

Lab Mission – To discover, develop, and deliver novel therapies for the treatment of corneal trauma and diseases.

– Determine if Prolactin Induced Protein (PIP) is a biomarker for keratoconus.

– Delineate the role of sex hormones during the onset and progression of keratoconus.

– Investigate and delineate the role of sphingolipids in corneal wound healing, using complementary in vitro and in vivo models.

– Investigate and determine the role of Peroxisome Proliferator-Activated Receptor-α in diabetic keratopathy, using in vitro and in vivo models.

RaghuRaghu 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.

CameronCameron 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.


DorotaDorota Stankowska, PhD

Assistant Professor

My research focusses on mechanisms underlying the neuroprotective effects of transcription factor Brn3b in a rat model of ocular hypertension. Our studies have shown that following elevated intraocular pressure (IOP) mediated axonal injury in rats, administration of rAAV-Brn3b, promotes neuroprotection of retinal ganglion cells and optic nerve axons. Additionally, intravitreal rAAV-Brn3b administration significantly restored the visual acuity in IOP-elevated rat eyes. The long term goals are to uncover novel molecular targets of Brn3b and explore their potential to be developed as neuroprotective agents for the treatment of glaucoma.


HongliHongli 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.

Iok-Hou Pang, PhD


Dr. Pang’s research interests mainly focus on the understanding of glaucoma etiology, pathology, and pharmacology, especially on glaucoma neuroprotection.  His is working to delineate essential molecular and cellular mechanisms, as well as characterize receptors and signal transduction pathways related to the abnormal changes in glaucoma.  His laboratory is using rodents and primary cultures of retinal and optic nerve cells as study models to clarify biological events leading to the disease and its prevention and protection.

Thomas Yorio, PhD


Dr. Yorio’s laboratory focuses on glaucoma.  Areas of interest include aqueous humor dynamics, endothelin pharmacology in glaucoma, identifying potential targets for neuroprotection and in the area of glucocorticoid pharmacology and ocular hypertension, specifically on understanding the role of glucocorticoid receptor (GR) beta in dampening the ocular hypertensive response of glucocorticoids.