Shaw-Fang Yet, Ph.D.
Institute of Cellular and Systems Medicine
EDUCATIONPh.D., University of Houston, USA
M.S., National Taiwan University, Taiwan
B.S., National Taiwan University, Taiwan
PROFESSIONAL EXPERIENCESAssociate Investigator, Cardiovascular and Blood Medical Research Center, National Health Research Institutes, Taiwan (2007 – present)
Assistant Professor of Medicine, Brigham and Women’s Hospital/Harvard Medical School, USA (2004 – 2007)
Instructor in Medicine, Harvard Medical School, USA (2000 – 2004)
RESEARCH INTERESTSDr. Yet has a long-term interest in cardiovascular biology, particularly in two areas of research: oxidative stress associated pathophysiology in cardiovascular system and phenotypic modulation of vascular smooth muscle cells. Recently, Dr. Yet has developed new interest in stem cell biology. Ongoing research projects are 1) investigating the mechanisms by which the cytoprotective gene heme oxygenase-1 exerts its protective functions, 2) determining the molecular mechanisms by which cysteine-rich protein 2 (CRP2) regulates vascular smooth muscle cell migration, 3) identifying regulatory modules that control vascular smooth muscle specific expression of CRP2, 4) investigating the signaling pathways involved in stem cell reprogramming processes and the pluripotency of stem cells using “induced pluripotent stem cell” system.
RESEARCH ACTIVITIES & ACCOMPLISHMENTSDr. Yet’s studies using heme oxygenase-1 null and transgenic mice have advanced current understanding of the cytoprotective functions of heme oxygenase-1 in cardiovascular biology. Dr. Yet’s laboratory was the first to demonstrate the in vivo function of cysteine-rich protein 2, an arterial smooth muscle cell protein, in vascular disease using genetically modified mice. Dr. Yet serves as a reviewer for several major scientific journals. Dr. Yet’s research projects are funded by a NHRI intramural grant and grants from National Science Council.
SELECTED PUBLICATIONS1.Tsui TY, Obed A, Siu YT, Yet S-F, Prantl L, Schlitt HJ, Fang ST. Carbon monoxide inhalation rescues mice from fulminant hepatitis through improving hepatic energy metabolism. Shock. 27:165-171, 2007.
2.Liu X, Pachori AS, Ward CA, Davis JP, Gnecchi M, Kong D, Zhang L, Murduck J, Yet S-F, Perrella MA, Pratt RE, Dzau VJ, Melo LG. Heme oxygenase-1 (HO-1) inhibits postmyocardial infarct remodeling and restores ventricular function. FASEB J. 20:207-216, 2006.
3.Wei J, Gorman, TE, Liu X, Ith B, Tseng A, Chen Z, Simon DI, Layne MD, Yet S-F*. Increased neointima formation in cysteine-rich protein 2–deficient mice in response to vascular injury. Circ Res. 97:1323-1331, 2005. (*=Corresponding Author)
4.Liu X, Wei J, Peng DH, Layne MD, Yet S-F*. Absence of heme oxygenase-1 exacerbates myocardial ischemia/reperfusion injury in diabetic mice. Diabetes. 54:778-784, 2005. (*=Corresponding Author)
5.Chang Y-F, Wei J, Liu X, Chen Y-H, Layne MD, Yet S-F*. Identification of a CArG-independent region of the cysteine-rich protein 2 promoter that directs expression in the developing vasculature. Am J Physiol Heart Circ Physiol. 285:H1675-1683, 2003. (*=Corresponding Author)
6.Yet S-F*, Layne MD, Liu X, Chen Y-H, Ith B, Sibinga NES, Perrella MA. Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling. FASEB J. 17:1759-1761, 2003. (*=Corresponding Author)
7.Yet S-F*, Tian R, Layne MD, Wang ZY, Maemura K, Solovyeva M, Ith B, Melo LG, Zhang L, Ingwall JS, Dzau VJ, Lee M-E, Perrella MA. Cardiac specific expression of heme oxygenase-1 protects against ischemia and reperfusion injury in transgenic mice. Circ Res. 89:168-173, 2001. (*=Corresponding Author)