Kenneth Walsh, Ph.D.
Professor of Medicine
Education:
Ph.D. – University of California, Berkeley
General field of research:
Cardiovascular Biology
Affiliations other than medicine:
Evans Center for Interdisciplinary Biomedical Research
Whitaker Cardiovascular Institute
Contact information:
Office
700 Albany Street, W611
Phone: (617) 414-2390
Lab
700 Albany Street, W619
Phone: (617) 414-2395
Fax: (617) 414-2391
Other research websites:
Research group information
Yuichi Akasaki, MD, PhD, Post-Doc – akasaki@bu.edu
Yasuhide Asaumi, MD, PhD, Post-Doc – yasaumi@bu.edu
Akiko Higuchi Ouchi, MD, Post-Doc – akih@bu.edu
Jesse Lugus, PhD, Post-Doc – jjlugus@bu.edu
Kazuto Nakamura, MD, PhD, Post-Doc – kazdoc@bu.edu
Koji Ohashi, MD, PhD, Post-Doc – ohashik@bu.edu
Noriyuki Ouchi, MD, PhD, Assistant Professor – nouchi@bu.edu
Kyriako Papanicolaou, Graduate Student – kyriakos@bu.edu
Jennifer Parker, Graduate Student – jparker@bu.edu
Taina A. Rokotuiveikau (tech) – trokotui@gmail.com
Masayuki Shimano, MD, PhD, Post-Doc – mshimano@bu.edu
Ling Zeng, Graduate Student lingz@bu.edu
Keywords:
Cardiovascular; Cell Cycle; Glucose Metabolism; Obesity; Myokine
Summary of research interest:
Research in the Walsh laboratory focuses on signaling- and transcriptional-regulatory mechanisms that control normal and pathological tissue growth in the cardiovascular system. Many of these studies involve analyses of the PI3-kinase/Akt/GSK/Forkhead signaling axis, which is of critical importance in the regulation of organ growth and body size. Signaling through this pathway controls cellular enlargement (hypertrophy), cell death (apoptosis), and blood vessel recruitment and growth (angiogenesis). We have shown that the PI3-kinase/Akt/GSK/Forkhead signaling axis regulates multiple steps critical in angiogenesis including endothelial cell apoptosis, differentiation, nitric oxide production and migration, that some of these signaling steps are important for cardiac hypertrophy during normal postnatal development, and that they regulate myocyte survival in models of heart disease.
A related project analyzes the impact of metabolic dysfunction on cardiovascular tissues. It is now recognized that adipose tissue functions as an endocrine organ and that obesity contributes to cardiovascular and metabolic disorders through an imbalance of cytokines. Adiponectin is an adipocyte-derived cytokine that is down-regulated in obese individuals. Hypo-adiponectinemia is an independent risk factor for the development of diabetes, hypertension and coronary artery disease. We have found that adiponectin has beneficial actions on the cardiovascular system by directly acting on heart and blood vessels.
Recent publications:
Ohashi K., N. Ouchi, K. Sato, A. Higuchi, T. Ishikawa, H.R. Herschman, S. Kihara, K. Walsh. 2009. Adiponectin promotes revascularization of ischemic muscle through a COX-2 dependent mechanism. Mol. Cell. Biol. [Epub ahead of print].
Oshima Y., N. Ouchi, K. Sato, Y. Izumiya, D.R. Pimental, K. Walsh. 2008. Follistatin-like 1 is an Akt-regulated cardioprotective factor that is secreted by the heart. Circulation 117: 3099-3108.
Izumiya Y., T. Hopkins, C. Morris, K. Sato, L. Zeng, J. Viereck, J.A. Hamilton, N. Ouchi, N, K. LeBrasseur, K. Walsh. 2008. Fast/glycolytic muscle fiber growth reduces fat mass and improves metabolic parameters in obese mice. Cell Metab 7: 159-172.
Takemura Y. , N. Ouchi, R. Shibata, T. Aprahamian, M.T. Kirber, R.S. Summer, S. Kihara, K. Walsh. 2007. Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. J. Clin. Invest. 117: 375-386.
Shibata R., K. Sato, D.R. Pimental, Y. Takemura, S. Kihara, K. Ohashi, T. Funahashi, N. Ouchi, K. Walsh. 2005. Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2- dependent mechanisms. Nature Med. 10:1096-1103.
Shiojima I., K. Sato, Y. Izumiya, S. Schiekofer, M. Ito, R. Liao, W.S. Colucci, K. Walsh. 2005. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J. Clin. Invest. 115:2108-2118.
Shibata R., N. Ouchi, M. Ito, S. Kihara, I. Shiojima, D.R. Pimentel, M. Kumada, K. Sato, S. Schiekofer, K. Ohashi, T. Funahashi, W.S. Colucci, K. Walsh. 2004. Adiponectin-mediated modulation of hypertrophic signals in the heart. Nature Med. 10:1384-1389.
Aprahamian T., I. Rifkin, B. Hugel, J.M. Freyssinet, K. Sato, J.J. Castellot, Jr., K. Walsh. 2004. Impaired clearance of apoptotic cells promotes synergy between atherogenesis and autoimmune disease. J. Exp. Med. 199:1121-1131.
