Phone:
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Office:
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(973) 972-8619
(973) 972-8919
MSB I-576
sadoshju@umdnj.edu
(973) 972-8919
MSB I-576
sadoshju@umdnj.edu
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Junichi Sadoshima MD, PhD
| Biography: MD, Kyushu University, Fukuoka, Japan -1983 PhD, Kyushu University, Fukuoka, Japan -1989 Postdoctoral Fellow, Beth Israel Hospital, Harvard Medical School, Boston, MA 1990 -1994 Assistant Professor, University of Michigan, Ann Arbor, MI 1994 -1998 Allegheny University of the Health and Sciences, Pittsburgh, PA 1998 - 2000 Associate Professor, UMDNJ-NJ Medical School, Newark, NJ 2000 - 2003 Professor, UMDNJ-NJMS, Newark, NJ 2003 - present Vice Chair, Department of Cell Biology and Molecular Medicine, UMDNJ-NJMS, Newark, NJ 2005 - 2010 Executive Director, Cardiovascular Research Institute, UMDNJ-NJMS, Newark, NJ 2010 - present Interim Chair, Department of Cell Biology and Molecular Medicine, UMDNJ, 2011 |
| Editorial Board: Circulation Research - Top Reviewer 2009 Antioxidants and Redox Signaling American Journal of Physiology - Heart and Circ Editorial Team 2010 Journal of Cardiovascular Pharmacology Journal of Molecular and Cellular Cardiology - Top Reviewer 2009-2010 Autophagy Journal of Clinical Investigation Circulation Journal Journal of Cardiovascular Translational Research American Journal of Physiology |
| Fellow: American Heart Association (AHA) International Society of Heart Research (ISHR) Member: American Society for Clinical Investigation (ASCI) |
| Introduction of Dr. Sadoshima's lab and auto-activation of AT1 receptor-signaling and hypertrophy in response to mechanical stretch. Over the decades, his laboratory has continued to conduct seminal research into the regulators of cell death, survival, and growth, including major studies of the roles of glycogen synthase kinase 3-beta-Mst-1, mitogen-activated protein kinases, sirtuins, and other factors. One thrust of his recent research has been the role of reactive oxygen species and oxidative stress on both survival and hypertrophic stimulation. His laboratory first established the central role of the key reductive protein thioredoxin-1, in this regulation, and led the field in showing the mechanisms of its control. Most recently, he showed a novel mechanism whereby thioredoxin-1 regulates the oxidation of transcription factors (class II histone deacetylases), providing the first direct link between oxidative stress and a mechanism for cardiac hypertrophy. His highly creative work has forged many new and important pathways that have become subsequent targets of research world wide. (From the Ira and Jean Belfer Lectureship at Johns Hopkins School of Medicine, May 2009) |
Best Consulting Editor 2011