main interest in my lab is understanding the molecular mechanisms
that regulate cardiac growth, both proliferative and hypertrophic.
We extensively use genetic murine models in an attempt to correlate
molecular insights with whole organ physiology. The long-term goal
of my research is to determine the consequences of the cardiac
myocyte cell cycle exit in diseases such as congestive heart failure
and understand how hypertrophic growth can lead to left ventricular
failure. Ultimately, we hope to identify molecular targets that
would allow targeted therapy to regenerate myocardium.
MacLellan, W.R., Xiao, G., Abdellatif, M., and Schneider, M.D.
(2000) A novel Rb- and p300-binding protein regulates
transactivation by MyoD. Mol. Cell. Biol. 20(23):8903-8915.
MacLellan, W.R, and Schneider, M.D. (2000) Genetic dissection of
cardiac growth control pathways. Ann. Rev. Physiol. 62:289-319.
MacLellan, W.R., (2000) Advances in the molecular mechanisms of
heart failure. Curr. Opin. Card. 15:128-135.
Sivasubramanian, N., Coker, M., Kurrelmeyer, K., MacLellan, W.R.,
DeMayo, F., Spinale, F.G., and Mann, D.G. (2001) Left ventricular
remodeling in transgenic mice with cardiac-restricted overexpression
of tumor necrosis factor. Circulation, 104(7):826-831.
Horwich, T., Fonarow, G.C., Hamilton, MA, MacLellan, W.R.,
Woo, M., Tillisch, J. (2001) The relationship between obesity and
mortality in patients with heart failure. J. Am. Coll Card.
Xiao, G., Mao, S., Baumgarten, G.,
Serrano, J., Jordan, M., Roos, K., Fishbein, M., and MacLellan,
W. R. (2001) Inducible activation of c-Myc in adult myocardium
in vivo provokes cardiac myocyte hypertrophy and reactivation of DNA
synthesis. (in press).