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Alessandro Arduini

Publications

Yang L, Calay ES, Fan J, Arduini A, et al. S-Nitrosylation links obesity-associated inflammation to endoplasmic reticulum dysfunction. Science. 2015;349(6247):500-506.

Arduini A, Serviddio G, Escobar J, et al. Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions. Am J Physiol Gastrointest Liver Physiol. 2011;301(1):G119-G127.

Gomez-Cabrera MC, Domenech E, Romagnoli M, et al. Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. Am J Clin Nutr. 2008;87(1):142-149.

Alessandro Arduini, Ph.D

Alessandro Arduini is a research scientist, working under the direction of Sekar Kathiresan and Patrick Ellinor in the Cardiovascular Disease Initiative (CVDi), part of the Broad–Bayer Collaboration at the Broad Institute of MIT and Harvard. Within the program, he is team leader on projects that aim to link genetic variants to cardiovascular disease and identify novel therapeutic interventions. His research interests lie in the link between nutrients and cellular and organelle stress in the context of metabolic and inflammatory diseases. Throughout his career, he elucidated some mechanistic aspects of sensing, signal transduction, and stress responses relevant to human disease, using either cellular and animal models, or human patients.

Arduini joined the Broad Institute in 2017 after post-doctoral training in the Harvard T.H Chan School of Public Health. Under the mentorship of Gokhan Hotamisligil, he elucidated novel roles of the immune sensor PKR in inflammation in the context atherosclerosis, and contributed to the mechanistic understanding of IRE-1 dysfunction in obesity and the critical role of NRF-1 in cholesterol homeostasis. He later joined the Mitchell lab where he studied a novel connection between nutrients, endothelial cell metabolism, and angiogenesis. Arduini’s interests for metabolic alterations and metabolic reprogramming during cellular phenotypic alterations stem from his graduate work in the area of mitochondrial dysfunction and redox biology in models of obstructive jaundice and pancreatitis under the direction of Juan Sastre at the University of Valencia, Spain.

Arduini obtained his Ph.D. in physiology at the School of Medicine of the University of Valencia (Spain). His full list of contributions encompasses research in obesity, non-alcoholic steato-hepatitis, diabetes, atherosclerosis, vascular biology, obstructive jaundice, prematurity, and exercise.

Contact Alessandro Arduini via email at aarduini@broadinstitute.org.

March 2018