Dr. Sima Tarzami, Ph.D.

Contact information

Office Location: Seeley G. Mudd Building Room 329
Office Telephone: 202-806-5269
Laboratory Location: Adams Building Room 2518C


B.A., Hofstra University, New York (1992)
M.S., Hofstra University, New York (1995)
Ph.D., Albert Einstein College of Medicine, New York (2002)
Postdoctoral Fellow, Eli Lilly Pharmaceutical Company (2004-2006)
Postdoctoral Fellow, Albert Einstein College of Medicine (2006-2008)


Cell and Molecular Biology
Cardiac Physiology and Pharmacology


My laboratory studies the role of chemokines on cardiac myocyte biology. We focus on cardiac physiology in both in vitro and in vivo models of heart failure targeting specific signaling pathways. We have demonstrated that chemokines, once thought to act only on inflammatory cells, can elicit biological responses from cardiac myocytes. This line of research is unique in bridging the areas of immunology (i.e. chemokines) and cardiovascular biology. Our focus is particularly on the CXCR4-CXCL12 regulation and signaling pathways in cardiac myocytes. The CXCR4-CXCL12 regulation and signaling pathways have been extensively studied in developmental processes, stem cell biology and in metastatic disease, focusing primarily on cells with a migratory phenotype. There is little known about CXCR4 signaling in cardiac myocytes. Our studies suggest that under conditions of stress, the paracrine and/or autocrine activation of CXCR4 by its ligand may trigger intracellular signaling pathways which may exacerbate contractile dysfunction. We have demonstrated a clear interaction between CXCR4 and Beta-2 adrenergic receptor and that CXCR4 activation can interfere with Beta adrenergic receptor downstream signaling. In the light of Beta adrenergic importance in progression of heart failure, we have set to examine the mechanistic role of CXCL12-CXCR4 in the pathophysiology of heart disease.

Focus Areas

Chemokines and Heart disease: Adaptive or Maladaptive
Beta-2 adrenergic-mediated cardiac dysfunction
L type Ca channels activity and heart function
Cardiac hypertrophy and failure

Grants and Funding Awards

National Heart, Lung, and Blood Institute (NHLBI) (2010-2013)
American Heart Association (2010-2013)
American Heart Association (2007-2010)


  1. Chen J, Chemaly E, Liang L, Kho C, Lee A, Park J, Altman P, Schecter AD, Hajjar RJ, Tarzami ST. Effects of   CXCR4 gene transfer on cardiac function following ischemia-reperfusion. Am J Pathol. 2010 Apr;176(4):1705-15.
  2. LaRocca T, Schwarzkopf M, Altman P, Zhang S, Gupta A, Gomes I, Alvin Z, Champion HC, Haddad G, Hajjar RJ, Devi LA, Schecter AD, Tarzami ST. B2 adrenergic receptor in the heart is modulated by interactions with CXCR4 chemokine receptor. J Cardiovasc Pharmacol. 2010 Nov;56(5):548-59.
  3. LaRocca TJ, Jeong D, Kohlbrenner E, Lee A, Chen J, Hajjar RJ, Tarzami ST. CXCR4 gene transfer prevents pressure overload induced heart failure.  J Mol Cell Cardiol. 2012 Aug;53(2):223-32.
  4. Larissa Lipskaia, Regis BOBE, Jiqiu Chen, Irene C. Turnbull, jose-javier lopez-barba, Elise Merlet, Dongtak Jeong, Ioannis Karakikes, Alexandra Ross, Lifan Liang, Nathalie Mougenot, Fabrice Atassi, Anne-Marie Lompre, Sima T Tarzami, Jason Kovacic, Evangelia Kranias, Roger Hajjar, and Lahouaria Hadri. Synergistic role of Protein Phosphatase Inhibitor 1 and SERCA2a in the acquisition of the Contractile Phenotype of Arterial Smooth Muscle Cells. Circulation. 2014 Feb 18;129(7):773-85.
  5. Wang ER, Jarrah AA, LaRocca TJ, Benard L, Chen J, Tarzami ST. Deletion of CXCR4 in cardiomyocytes exacerbates cardiac dysfunction following isoproterenol administration. Gene Ther. 2014 May;21(5):496-506.