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Mary Elizabeth Hartnett,  M.D., Ph. D., FACS, FARVO

Distinguée professeure d’ophtalmologie et de sciences visuelles
Titulaire de la Chaire Calvin S. et JeNeal N. Hatch Presidential Endowed en ophtalmologie et sciences visuelles
Directrice du service rétine pédiatrique au Moran Eye Center
Professeure adjointe en pédiatrie et en neurobiologie

John A. Moran Eye Center – University of Utah

Salt Lake City, Utah, ÉTATS-UNIS
courriel:  ME.Hartnett@hsc.utah.edu


Mary Elizabeth Hartnett, MD, holds the Calvin S. and JeNeal N. Hatch Presidential Endowed Chair in Ophthalmology and Visual Sciences and is a Distinguished Professor at the University of Utah. She is an adjunct professor at the University of Utah departments of Neurobiology and Pediatrics. Dr. Hartnett is the founder and director of Pediatric Retina at the John A. Moran Eye Center and principal investigator of the Retinal Angiogenesis Laboratory. She created the first-ever academic textbook on the subject, Pediatric Retina, in its third edition, which has proven to be an invaluable resource for residents and ophthalmologists internationally. Dr. Hartnett’s NIH-funded laboratory of vascular biology and angiogenesis has studied mechanisms causing pathology in age-related macular degeneration (AMD) and retinopathy of prematurity (ROP). Her work in AMD has been to understand the mechanisms involved in activation and invasion of choroidal endothelial cells anterior to the RPE in order to maintain vasculature that is physiologic and not damaging beneath the RPE. Her lab’s work in ROP provided the proof of concept to regulate an angiogenic signaling pathway by inhibiting VEGF to facilitate more normal intraretinal vascularization toward the ora serrata as well as to inhibit abnormal extraretinal neovascularization. She has translated her work through collaborations in protocol development of clinical trials. Dr. Hartnett has received numerous awards, including the Weisenfeld Award, the highest award for clinician-scientists given by the Association for Research in Vision and Ophthalmology (ARVO), in 2018, and is an ARVO Gold Fellow. She received the 2019 Paul Kayser/Retina Research Foundation Global Award, the Macula Society’s 2016 Paul Henkind Award and its 2019 Arnall Patz Medal, the Paul Kayser/RRF Global Award from the PanAmerica Society, and the 2021 Suzanne Veronneau-Troutman Award, the most prestigious award from Women in Ophthalmology. In 2022, she was one of six at the University of Utah to receive a distinguished research award, for Pediatrics and Ophthalmology. Dr. Hartnett’s prolific publication record includes 227 articles in peer-reviewed journals and over 40 book chapters. She has delivered numerous national and international invited lectures. Her long list of professional committee work includes serving as chair of the Publications Committee of ARVO, as a mentor for the ARVO Leadership Development Program, and in leadership positions internationally as chair of the research advisory committees for The Macula Society and the Jack McGovern Coats Disease Foundation as well as Chair of the Credentialing Committee for The Retina Society. She reviews manuscripts for more than 20 eye and science journals and serves on the editorial boards of PlosOne, Molecular Vision, and the American Journal of Ophthalmology. Dr. Hartnett is a Fellow of the American College of Surgeons (FACS) and a Silver and Gold Fellow of the Association for Research in Vision and Ophthalmology (FARVO).



Titre : Targeting pathologic signaling to restore homeostasis in age-related macular degeneration

Age-related macular degeneration (AMD) is a complex common disease that is influenced by genetic predisposition and external stresses, including those associated with aging. Our lab studies signaling effectors triggered by external stresses in choroidal endothelial cells and retinal pigment epithelium (RPE) that lead to features seen in advanced forms of AMD. We identified several important stresses, i.e., angiogenic, inflammatory and oxidative factors, that lead to activation of the GTPase, Rac1, and create feed-ford loops. Binding of active Rac1, Rac1GTP, to a multi-domain protein, IQGAP1, caused Rac1 to remain “on” further driving pathology. We identified another GTPase that interferes with pathologic steps to restore homeostasis of the outer retina.  In addition, we found that oxidized compounds within drusen lead to phenotypic changes in outer retinal cells, and we predict this occurrence may account for some of the cases of poor response to anti-VEGF agents. We study these processes in experimental models.