BBS Faculty Member - Anthony Rosenzweig

Anthony Rosenweig

Chief of Cardiology
Director of Research

Massachusetts General Hospital
Richard B. Simches Research Center, 3rd Floor
185 Cambridge Street
Boston, MA 02114
Tel: 617-724-1310

We are interested in why the heart fails. Heart failure is an enormous and growing cause of death and disability throughout the world. In addition, the heart provides a model system for studying fundamental cellular processes from cell growth and programmed death, to cell-lineage determination and regeneration.

Recently we’ve been interested in understanding how exercise protects the heart against heart failure. A variety of high throughput profiling techniques are being used to identify pathways differentially regulated in heart growth associated with exercise in comparison to the heart growth that precedes heart failure. These screens have identified interrelated transcriptional pathways (
Cell, 2010) and microRNA pathways (Cell Metabolism, 2015), which appear to mediate many of the phenotypic effects of exercise in vivo. In vivo gain- and loss-of-function models are being used to explore the functional effects and molecular mechanisms of this pathway in more detail.

We previously found that PI3-Kinase and Akt play important roles in cardiac growth and survival, as well as the response to exercise and disease. More recently we have been interested in another member of this family, the serine-threonine kinase SGK1, which is activated in diseased but not exercised hearts. We’ve found that genetic inhibition of SGK1 has profound protective effects in the heart, which has prompted a computational small molecule screen to identify SGK1 inhibitors. We are now interested in understanding the upstream and downstream pathways involved in SGK1’s effects in the heart.

Last Update: 8/6/2015


For a complete listing of publications click here.



Morissette, M.R., Stricker, J.C., Rosenberg, M.A., Buranasombati, C., Levitan, E.B., Mittleman, M.A., Rosenzweig, A. 2009. Effects of myostatin deletion in aging mice. Aging Cell 8:573-583.

C/EBPβ controls exercise induced cardiac growth and protects against pathological cardiac remodeling. Boström P, Mann N, Wu J, Quintero PA, Plovie E, Gupta R, Xiao C, MacRae CA, Rosenzweig A* and Spiegelman BM* (*contributed equally, co-corresponding).
Cell 2010;143:1072-1083.

Ashida N, Senbanerjee S, Kodama S, Foo SY, Coggins M, Spencer JA, Zamiri P, Shen D, Li L, Sciuto T, Dvorak A, Gerszten RE, Lin CP, Karin M, Rosenzweig A. IKK
b regulates essential functions of the vascular endothelium through kinase-dependent and -independent pathways. Nature Commun. 2011;2:318(1-9).

Platt, C.*, Houstis, N.*, Rosenzweig, A. Using exercise to measure and modify cardiac function.
Cell Metabolism 2015; 21(2): 227-36. PMCID: 4317572. *co-first authors; contributed equally.

Liu X*, Xiao J*, Zhu H, Wei X, Platt C, Damilano F, Xiao C, Bezzerides V, Boström P, Che L, Zhang C, Spiegelman BM, and Rosenzweig A. miR-222 is Necessary for Exercise-induced Cardiac Growth and Protects Against Pathological Cardiac Remodeling.
Cell Metabolism 2015; 21(4): 584-595. PMCID: 4393846. *co-first authors; contributed equally.

© 2015 by the President and Fellows of Harvard College