Dr. Zhang is a Postdoctoral Scholar at RabLab in the cardiopulmonary division. She has a PhD in Pharmacology from University of Rochester, NY. She has research in cardiovascular research and chronobiology published in high impact peer-reviewed journals. She is recipient of honors including predoctoral fellowship from AHA, Travel Grant for Early Career Investigators from Council on Arteriosclerosis, Thrombosis, and Vascular Biology. She has served as ad hoc reviewer for more than 40 manuscripts for reputed journals.

Honors & Awards

  • Invited speaker at CLIMB UP Research Symposium, State University of New York at Buffalo (2012)
  • Invited speaker and Outstanding Poster Presentation Award, Pharmacology and Toxicology Mini-Research Symposium, State University of New York at Buffalo (2014)
  • Invited speaker at Department of Pharmacology and Toxicology-Graduate Students Research Symposium, State University of New York at Buffalo (2014)
  • Master’s Student Best Poster Presentation Award, Upstate New York Pharmacology Society Annual Meeting (NYPS) (2015)
  • Latin Honors-summa cum laude for outstanding GPA, State University of New York at Buffalo (2015)
  • Invited speaker at Gordon Research Seminar on Cyclic-Nucleotide Phosphodiesterases (PDEs), Newry ME, Gordon Research Seminar (2018)
  • American Heart Association predoctoral fellowship, American Heart Association (2020)
  • ATVB Scientific Sessions Travel Grant for Early Career Investigators, American Heart Association (2021)
  • Vincent du Vigneaud Award, University of Rochester (2022)

Boards, Advisory Committees, Professional Organizations

  • Ad Hoc Reviewer, Bioscience Reports (2020 - Present)
  • Ad Hoc Reviewer, Clinical Science (2021 - Present)
  • Ad Hoc Reviewer, Journal of American Heart Association (2021 - Present)
  • Ad Hoc Reviewer, Frontiers in Cardiovascular Medicine (2022 - Present)
  • Member, American Society for Pharmacology and Experimental Therapeutics (ASPET) (2013 - 2015)
  • Member, American Heart Association (2019 - Present)

Professional Education

  • Doctor of Philosophy, University of Rochester (2022)
  • Master of Science, S.U.N.Y. State University at Buffalo (2015)
  • Master of Science, University of Rochester (2018)
  • Bachelor of Science, S.U.N.Y. State University at Buffalo (2015)
  • BS, State University of New York at Buffalo, Pharmacology (2015)
  • MS, State University of New York at Buffalo, Pharmacology (2015)
  • PhD, University of Rochester, Pharmacology (2022)

Stanford Advisors

All Publications

  • Reduced FOXF1 links unrepaired DNA damage to pulmonary arterial hypertension. Nature communications Isobe, S., Nair, R. V., Kang, H. Y., Wang, L., Moonen, J. R., Shinohara, T., Cao, A., Taylor, S., Otsuki, S., Marciano, D. P., Harper, R. L., Adil, M. S., Zhang, C., Lago-Docampo, M., Körbelin, J., Engreitz, J. M., Snyder, M. P., Rabinovitch, M. 2023; 14 (1): 7578


    Pulmonary arterial hypertension (PAH) is a progressive disease in which pulmonary arterial (PA) endothelial cell (EC) dysfunction is associated with unrepaired DNA damage. BMPR2 is the most common genetic cause of PAH. We report that human PAEC with reduced BMPR2 have persistent DNA damage in room air after hypoxia (reoxygenation), as do mice with EC-specific deletion of Bmpr2 (EC-Bmpr2-/-) and persistent pulmonary hypertension. Similar findings are observed in PAEC with loss of the DNA damage sensor ATM, and in mice with Atm deleted in EC (EC-Atm-/-). Gene expression analysis of EC-Atm-/- and EC-Bmpr2-/- lung EC reveals reduced Foxf1, a transcription factor with selectivity for lung EC. Reducing FOXF1 in control PAEC induces DNA damage and impaired angiogenesis whereas transfection of FOXF1 in PAH PAEC repairs DNA damage and restores angiogenesis. Lung EC targeted delivery of Foxf1 to reoxygenated EC-Bmpr2-/- mice repairs DNA damage, induces angiogenesis and reverses pulmonary hypertension.

    View details for DOI 10.1038/s41467-023-43039-y

    View details for PubMedID 37989727

    View details for PubMedCentralID 4737700