Andrius Kazlauskas, PhD
Professor
Department of Physiology and Biophysics
Ophthalmology and Visual Sciences
College of Medicine
Contact
Building & Room:
LIERI L221
Address:
1905 W. Taylor St, MC 648
Email:
Related Sites:
Lab Location
Building & Room:
LIERI L245
About
Investigation of the pathogenesis of blinding eye diseases such as diabetic retinopathy in order to improve current therapeutic option.
Research Currently in Progress
After a multi-decade period in academia, Dr. Kazlauskas closed his research lab at the Schepens Eye Research Institute/Harvard Medical School to transition to F. Hofmann-La Roche in Basel, Switzerland, where he joined the Department of Ophthalmology and contributed to the drug development process. In 2017 Dr. Kazlauskas re-started academic research focused on improving current approaches to managing patients with diabetic retinopathy. The lab is engaged in two research projects.
Pharmacosignaling in PDR
The goal of this project is to elucidate the molecular basis of anti-VEGF’s benefit in patients with proliferative diabetic retinopathy (PDR). The clinical observation that neutralizing VEGF reduces retinal edema and improves visual acuity in most patients, motivates us to investigate the underlying mechanism of this phenomenon. To this end, we are first identifying changes in gene expression and signaling events that are associated with anti-VEGF treatment in patients. The next step is to determine which of these changes are responsible for the therapeutic benefit. These discoveries will guide the design of alternative therapies for patients that do not fully benefit from existing anti-VEGFs. Furthermore, we will develop biomarkers that will improve our ability to diagnose susceptibility, monitor both disease progression, and the efficacy of intervention.
Targeting oxidative stress to prevent DR
Diabetes increases oxidative stress, which in endothelial cells compromises their barrier function and thereby contributes to diabetic retinopathy (DR). We are investigating diabetes-driven redox dysfunction in distinct subcellular compartments of endothelial cells in order to learn how to preserve barrier function of the retinal vasculature in patients who develop diabetes.