Takashi Matsui Laboratory
Takashi Matsui, MD, PhD
Cardiovascular Research, Cardiovascular Division
Beth Israel Deaconess Medical Center
3 Blackfan Circle, E/CLS #907
Boston MA 02215
Tel: 617-735-4241
e-mail:
tmatsui@bidmc.harvard.edu
Education/Training/Appointments:
Dr. Matsui received a medical degree from Jikei University School of Medicine in Tokyo JAPAN in 1986 and a PhD from Dept of Pharmacology, Jikei University in 1992. He completed his residency before receiving his PhD and went on to serve as assistant in cardiology in Jikei University until coming to the US. In 1995, he joined at Mass General Hospital (MGH) Cardiovascular Research Center as a research fellow. After Dr. Matsui went on to serve as instructor in medicine in MGH, Harvard Medical School (HMS) from 1999 to 2006 and in Beth Israel Deaconess Medical Center (BIDMC) in 2006, he has joined the HMS faculty as assistant professor of medicine in Cardiovascular Research, Cardiovascular Division, BIDMC.
Research Interests:
Heart failure is a leading cause of hospitalization and mortality in the US. Dr. Matsui and his colleagues focus on understanding the mechanism behind cardiac dysfunction arising from myocardial infarction and cardiac hypertrophy, apparent risk factors for heart failure. Specifically, Dr. Matsui's interests center around the role of the mammalian target of rapamycin (mTOR) in cell survival, cardiac hypertrophy and remodeling. In order to investigate the role of mTOR in the heart, Dr. Matsui and his colleagues utilize a variety of in vitro, in vivo, and ex vivo models. Recombinant DNA is employed in both cells via the use of gene transfer and animals via the generation of transgenic mice. In fact, Dr. Matsui and his colleagues are studying mice engineered with cardiac-specific overexpression of mTOR in order to see if changes in disease processes related to heart failure occur. Several stresses including ischemia-reperfusion and pressure-overload are employed in order to mimic disease states. Hopefully, an enhanced comprehension of the mechanism responsible for cardiac dysfunction will lead to the identification of novel therapeutic targets for the treatment of heart failure.
Highlighted Recent Publications:
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Matsui T, Li L, del Monte F, Fukui Y, Franke TF, Hajjar RJ, Rosenzweig A. Adenoviral gene transfer of activated PI 3-kinase and Akt inhibits apoptosis of hypoxic cardiomyocytes
in vitro.
Circulation 1999;100:2373-2379.
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Matsui T, Tao J, del Monte F, Lee K-H, Li L, Picard M, Force TL, Franke TF, Hajjar RJ, Rosenzweig A. Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia
in vivo.
Circulation 2001;104:330-5
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Matsui T, Li L, Wu JC, Cook SA, Nagoshi T, Picard MH, Liao R, Rosenzweig A. Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart.
J Biol Chem 2002;277:22896-90
- Nagoshi T,
Matsui T, Aoyama T, Leri A, Anversa P, Li L, Ogawa W, Federica del Monte F, Judith K Gwathmey JK, Grazette L, Hemmings B, David A. Kass DA, Champion HC and Rosenzweig A. PI3K rescues the detrimental effects of chronic Akt activation in the heart during ischemia-reperfusion injury.
J Clin Invest 2005;115:2128-38
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Matsui T, Nagoshi T, Hong EG, Luptak I, Hartil K, Li L, Gorovits N, Charron MJ, Kim JK, Tian R, Rosenzweig A. The effects of chronic Akt activation on glucose uptake in the heart.
Am J Physiol Endocrinol Metab. 2006;290:E789-97
Dr. Matsui's Research
Dr. Matsui's Publications
Dr. Matsui's Lab Members Dr. Matsui's Contacts