Sally Radovick, MS, MD, is a Professor of Pediatrics and Director of the Clinical and Translational Research Institute at the University of Arizona. She received her medical degree from Northeastern Ohio Universities College of Medicine, USA, completed her residency in pediatrics at Case Western Reserve University, USA, and her fellowship in pediatric endocrinology at the National Institutes of Health (NIH). She has been a faculty member at Case Western Reserve University, Harvard Medical School, The University of Chicago, and Johns Hopkins University, most recently at Rutgers, Robert Wood Johnson Medical School.
Dr. Radovick specializes in pediatric diabetes, growth, development, and pubertal disorders in children. She has conducted biomedical research and mentored students and fellows for 30 years, mentoring over 75 graduate students, postdoctoral fellows, and early career faculty. She also received NIH funding as a mentor for 26 postdoctoral mentees, including 7 NRSAs and 15 K01, K08, or K23s. She also received a K24 for career development. Previously, she was the Director of the Division of Pediatric Endocrinology and the PI of the T32 Training Program in Molecular and Cellular Endocrinology at Johns Hopkins. She was also the Director of the pilot and feasibility (P and F) core of the NIDDK Diabetes Research Center (DRC) and the NIDDK-sponsored medical student summer program in diabetes research. Additionally, as the Vice-Chair for Research in the Department of Pediatrics, she was the Director of the T32 training program for residents and fellows in Pediatrics. As the Chief of Pediatric Endocrinology at the University of Chicago, she was the Associate Program Director for its Integrated T32 in Endocrinology. In 2004, Dr. Radovick was awarded the first T32 in Chicago designed to train Pediatric Endocrinologists. Most recently, she was the PI of the Rutgers CTSA KL2 program.
Her research is focused on determining the regulation of the gonadotropin-releasing hormone (GnRH) gene, which has a central role in controlling the onset of puberty. Her group was the first to generate GnRH-expressing neuronal cell lines and in vitro map the cellular regulation of this critical gene. She has developed genetically modified mouse models to elucidate mechanisms of in vivo regulation of GnRH secretion in response to neuroendocrine stimulation and sex steroid feedback regulation. With recent evidence that implicates the neuroendocrine protein kisspeptin in pubertal onset and reproductive cycling, she has extended her studies of neuroendocrine sex steroid regulation to kisspeptin. These studies have implicated kisspeptin in mediating peripheral metabolism and as a ‘missing link’ between reproductive dysfunction and obesity. The results of this research long term provide insights into pubertal disorders and PCOS, as well as future therapies for infertility.
The other central research area has been to characterize the transcription factors essential for normal pituitary development. Her initial studies provided the first genetic mechanism of a child with short stature due to hypopituitarism; this involved a mutation in the POU-1F1 (Pit-1) gene necessary for pituitary cell lineage determination and differentiation. Understanding the hypothalamic-pituitary regulation of growth has led to insights into the relationship between linear growth, glucose metabolism, and obesity. She is also a co-investigator on epidemiologic studies to determine the long-term metabolic effects of premature birth.
The NIH has continuously supported these studies since 1992, including an R01 to determine the role of sex steroids in puberty and reproductive cycling and a U01 collaborative agreement with investigators at the NIH Clinical Center to determine the genetics of short stature. She has been a member of many NIH study sections and was the previous chair of the Integrative and Clinical Endocrinology and Reproduction Study Section (ICER).