Carol A. Eisenberg, Ph.D., joined the Department of Physiology at New York Medical College in 2008, following 13 years on the faculty at the Medical University of South Carolina. Dr. Eisenberg's scientific career has always included a strong emphasis as educator, administrator, and researcher. At NYMC, she has served as research advisor for postdoctoral fellows, thesis advisor for Ph.D. and  M.S. students, as well as lab supervisor for numerous students from medical, undergraduate, and secondary schools. Administrative activities have included serving as chair of the GSBMS Course Evaluation Committee and as a member of the GSBMS Ph.D. Admissions and Touro College of Dental Medicine Student Academic Performance and Review (2019-) Committees.

Dr. Eisenberg has been a principal investigator for over 25 years, investigating stem cell differentiation in the embryonic and adult heart. Her research focus is on signaling mechanisms that underlie how myocardial cell health is maintained in the adult.

Education

  • Ph.D., Cell Biology, Cornell University Medical College
  • M.S., Villanova University
  • B.S./B.A., Biology, French, Cabrini College
  • Postdoctoral Training, Cell Biology & Anatomy, Medical University of South Carolina

Research

Dr. Eisenberg's research focus is on the signaling mechanisms that underlie how myocardial cell health is maintained in the adult heart. This topic is investigated in her laboratory from three distinct but overlapping vantage points. The first project examines signaling pathways activated in the diseased heart using the tgG6/lacZ mouse model. The tgG6/lacZ transgenic mouse expresses a β-galactosidase (lacZ) reporter driven by a specific enhancer of the GATA-6 gene, and which serves as a marker for the re-emergence of a fetal gene program in the heart under conditions of stress and disease. The second project involves the development of culture conditions that allow for the long-term maintenance of fully differentiated myocardial tissue in culture, as the means for understanding how the cardiac cells continues to sustain their viability and functional activity. The final project looks at the cell and molecular events guiding the differentiation of stem cells for replacement cardiomyocytes. These three areas of study are complementary to the laboratory’s overall goal of understanding how the functional capabilities of the adult heart can be preserved throughout life.

Publications

  • Eisenberg LM, Eisenberg CA. "Stem Cells Associated with Adult Skeletal Muscle Can Form Beating Cardiac Tissue In Vitro in Response to Media Containing Heparin, Dexamethasone, Growth Factors and Hydrogen Peroxide." International journal of molecular sciences, 26(6), (2025) . doi: 10.3390/ijms26062683
  • Tartaglia JT, Eisenberg CA, DeMarco JC, et. al. "Mobilization of Endogenous CD34+/CD133+ Endothelial Progenitor Cells by Enhanced External Counter Pulsation for Treatment of Refractory Angina." International journal of molecular sciences, 25(18), (2024) . doi: 10.3390/ijms251810030
  • Mitry MA, Laurent D, Keith BL, et. al. "Accelerated cardiomyocyte senescence contributes to late-onset doxorubicin-induced cardiotoxicity." American journal of physiology. Cell physiology, 318(2), (2020) C380-C391. doi: 10.1152/ajpcell.00073.2019
  • Eisenberg CA, Eisenberg LM. "A Consideration of the Non-Pregnant Human Uterus as a Stem Cell Source for Medical Therapy." Current stem cell research & therapy, 14(1), (2019) 77-78. doi: 10.2174/1574888X1401181217130033
  • Borghetti G, Eisenberg CA, Signore S, et. al. "Notch signaling modulates the electrical behavior of cardiomyocytes." American journal of physiology. Heart and circulatory physiology, 314(1), (2018) H68-H81. doi: 10.1152/ajpheart.00587.2016
  • Yang J, Kaur K, Edwards JG, et. al. "Inhibition of Histone Methyltransferase, Histone Deacetylase, and β-Catenin Synergistically Enhance the Cardiac Potential of Bone Marrow Cells." Stem cells international, 2017(), (2017) 3464953. doi: 10.1155/2017/3464953
  • Kaur K, Yang J, Edwards JG, et. al. "G9a histone methyltransferase inhibitor BIX01294 promotes expansion of adult cardiac progenitor cells without changing their phenotype or differentiation potential." Cell proliferation, 49(3), (2016) 373-85. doi: 10.1111/cpr.12255
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