Donna Zhang,

Dr. Donna D. Zhang, Ph.D., is a distinguished molecular toxicologist renowned for her groundbreaking research in understanding the mechanisms underlying various diseases and developing innovative therapeutic strategies. She earned her Ph.D. in Molecular Toxicology from New York University’s Nelson Institute of Environmental Medicine in 1997, focusing on the identification and characterization of the novel gene Cap43 induced by Ni2+ compounds. Throughout her illustrious career, she has held several esteemed academic positions, including her current role as the Dr. Herbert A. Wertheim Professor at the Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology at the University of Florida. Prior to this, Dr. Zhang served as the Musil Family Endowed Chair in Drug Discovery at the College of Pharmacy at the University of Arizona, where she made significant contributions to the field through her research and teaching.

With a passion for education and mentorship, Dr. Zhang has made significant contributions to the field through her teaching and supervision of Ph.D. students. She has developed and coordinated various courses in pharmacology and toxicology, shaping the next generation of scientists and pharmacists. Additionally, she actively engages in service and outreach activities both within her institution and externally, serving on numerous committees and review panels for prestigious organizations such as NIH and the Society of Toxicology. Dr. Zhang’s dedication to advancing scientific knowledge and her commitment to training future leaders in the field underscore her invaluable contributions to the scientific community.

My research endeavors explore the intricate mechanisms of NRF2 redox biology, the pathogenesis of arsenic, and the development of preclinical drugs targeting NRF2. The goal is to leverage the body’s own defense systems, particularly the NRF2 pathway, to combat human diseases. NRF2, a pivotal transcription factor, orchestrates the cellular defense against environmental insults by regulating genes critical for maintaining redox and metabolic homeostasis.

Since NRF2’s discovery, it has been championed for its protective role against oxidative stress. Nonetheless, research from my laboratory has exposed its paradoxical role in cancer progression and therapy resistance. Our recent pioneering work has linked NRF2 high expression in certain cancers to enhanced survival and resistance to a new class of cell death, ferroptosis. These studies have significant implications, as NRF2 inhibition could transform therapeutic approaches for treatment-resistant cancers.

Additionally, my team’s research has implicated persistent NRF2 activation in the carcinogenic and diabetogenic effects of arsenic, a notorious environmental toxin affecting millions globally. This has set the stage for the development of specific NRF2 inhibitors, a yet unmet need in the field, to dissect NRF2’s detrimental roles in disease.

In summary, my lab’s efforts are directed towards: Unraveling the NRF2 signaling network. Deciphering NRF2 dysregulation in arsenic-induced carcinogenesis and diabetes. Developing NRF2-centric therapeutic strategies, including small molecules and nanobodies. Investigating the molecular biology of the CNC family proteins (NRF1, NRF2, and NRF3). The ultimate aim is to mitigate the impact of diseases exacerbated by environmental factors like arsenic, through innovative NRF2-targeted interventions.

0000-0002-8972-697X

• Cancer
• Diabetes
• Ferroptosis
• NRF2
• NRF2-Keap-ARE pathway
• arsenic toxicity
• autophagy
• redox biology