Vishwa Deep Dixit
Professor, Yale School of Medicine
Vishwa Deep Dixit studied veterinary medicine in Hisar, India, completed PhD research at the University of Hannover, Germany, and conducted postdoctoral research at the U.S. National Institute on Aging (NIA) in Baltimore. Among his lab’s notable findings, Dixit and colleagues established that the NLR family pyrin domain–containing 3 (NLRP3) inflammasome is a key driver of inflammaging; reducing NLRP3 activity in animal models mitigates cognitive deficits, adipose dysfunction, immunosenescence, and thymic aging. NLRP3 inhibitors are now in Phase 2 clinical testing.
Working at the interface of metabolism and immunology, the Dixit lab showed that ketone bodies function as endogenous immunometabolic brakes that deactivate the inflammasome, and that elevating the pro-longevity hormone FGF21 protects against thymic involution, immune dysfunction, and organismal aging. In humans undergoing moderate calorie restriction in the CALERIE trial, the lab identified inflammaging targets—including SPARC, PLA2G7, complement C3a reduction, and cysteine metabolism—linked to healthspan regulation. More recently, Dixit’s laboratory discovered that nerve-associated macrophages (NAMs) modulate sympathetic nervous system activity and adipose inflammaging. Ongoing work is investigating the golden spiny mouse as a model of resilient aging to identify actionable inflammaging checkpoints.
Dixit is a member of the Academy for Health and Lifespan Research and the Connecticut Academy of Science and Engineering. He has published more than 100 papers in leading scientific journals, and his contributions have been recognized with multiple honors, including a Glenn Award and the NIA’s 2017 Nathan Shock Award for pioneering work on the immunobiology of aging.
Working at the interface of metabolism and immunology, the Dixit lab showed that ketone bodies function as endogenous immunometabolic brakes that deactivate the inflammasome, and that elevating the pro-longevity hormone FGF21 protects against thymic involution, immune dysfunction, and organismal aging. In humans undergoing moderate calorie restriction in the CALERIE trial, the lab identified inflammaging targets—including SPARC, PLA2G7, complement C3a reduction, and cysteine metabolism—linked to healthspan regulation. More recently, Dixit’s laboratory discovered that nerve-associated macrophages (NAMs) modulate sympathetic nervous system activity and adipose inflammaging. Ongoing work is investigating the golden spiny mouse as a model of resilient aging to identify actionable inflammaging checkpoints.
Dixit is a member of the Academy for Health and Lifespan Research and the Connecticut Academy of Science and Engineering. He has published more than 100 papers in leading scientific journals, and his contributions have been recognized with multiple honors, including a Glenn Award and the NIA’s 2017 Nathan Shock Award for pioneering work on the immunobiology of aging.