BBS Faculty Member - Anthony Rosenzweig

Anthony Rosenweig

Director, Cardiovascular Research
Associate Chief of Cardiology

Beth Israel Deaconess Medical Ctr
Center for Life Sciences - CLS-947
3 Blackfan Circle
Boston, MA 02215
Tel: 617-735-4200
Fax: 617-735-4202
Email: arosenzw@bidmc.harvard.edu



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. A recently identified transcriptional pathway involved C/EBP
β and CITED4 not only reproduces many of the effects of exercise and protects the heart from heart failure, but appears to enhance the heart’s regenerative capacity. 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. Other ongoing studies are investigating cardiac micro-RNAs regulated by exercise and their potential protective effects in the heart. As part of an NIH-funded proteomics consortium that includes investigators from the Broad, MGH, and BWH, we are also investigating the cardiac phospho-proteome and its role in cardiac disease.

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.

More recently, we have begun to use human iPS cells as a cellular model. Ultimately iPS-derived cardiomyocytes may provide patient-specific models in which we can study cellular mechanisms and test therapeutic approaches.



Last Update: 8/22/2013



Publications

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.

Rosenzweig, A. Illuminating the Potential of Pluripotent Stem Cells.
N Engl J Med 2010; 363:1471-1472.

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.

Bezzerides V, Rosenzweig A. Saying yes to exercise and no to cardiac injury.
Circ Res. 2011;108:1414-1416.

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).



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