Kathryn J. Moore
New York University
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Primary Section: 61, Animal, Nutritional, and Applied Microbial Sciences Secondary Section: 42, Medical Physiology and Metabolism Membership Type:
Member
(elected 2021)
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Biosketch
Dr. Moore is recognized for her work on the molecular mechanisms of immuno-metabolic interactions. Her discoveries have provided fundamental insights into responses to cholesterol and nutrient excess resulting in vascular and metabolic inflammation, including pathways regulating cholesterol homeostasis and inappropriate activation of innate immune signaling. Moore was born in Montreal, Canada, where she attended McGill University, earning a bachelor’s degree in microbiology in 1989 and a Ph.D. in parasitology in 1994. She moved to Boston to pursue postdoctoral training at Brigham and Women’s Hospital in autoimmunity and Massachusetts General Hospital in vascular biology, and joined the faculty of Harvard Medical School in 2001. She moved to New York University Grossman School of Medicine in 2009, where she directs the Cardiovascular Research Center. Moore is a passionate advocate for increasing diversity in science and mentoring the next generation of investigators.
Research Interests
Kathryn Moore’s laboratory focuses on understanding how metabolic stressors drive chronic inflammatory responses and disease pathogenesis. Her early work helped establish how altered-self ligands that accumulate in diseases of aging (atherosclerosis, Alzheimer’s disease) trigger innate immune signaling pathways to drive pathogenic inflammatory responses. Her work has defined fundamental mechanisms through which oxidized lipids and amyloid proteins activate Toll-like receptors and inflammasomes, and described new roles for neuronal guidance cues in directing immune cell function. More recently, her groundbreaking research on how noncoding RNAs regulate the response to cholesterol excess has revealed fundamental mechanisms by which humans maintain lipid homeostasis and host defense against pathogens. She identified microRNA-33 as a regulator of plasma HDL cholesterol levels, and unveiled key roles for this and other microRNAs, as well as long noncoding RNAs, in coordinating cellular and systemic lipid metabolism and immune responses. Together, these studies have forged new links between lipids, metabolism and innate immunity to reveal fundamental insights into the pathogenesis of atherosclerosis and other sterile inflammatory conditions.
