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Marlene Rabinovitch

Academic Appointments

  • Dwight and Vera Dunlevie Professor in Pediatric Cardiology

Contact Information

  • Clinical Offices
    Stanford University School of Medicine 269 Campus Dr CCSR Room 1215A MC 5162 Stanford, CA 94305
    Tel Work (650) 723-8239 Fax (650) 723-6700
  • Academic Offices
    Personal Information
    Alternate Contact
    Michelle Fox Administrative Associate Tel Work 723-8239
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Cardiology (Heart), Pediatric
  • Pediatric Cardiology

Academic Appointments

Administrative Appointments

  • Director of Research, Vera Moulton Wall Center for Pulmonary Vascular Disease (2003 - present)

Honors and Awards

  • Judith Pool Mentoring Award, Northern California Chapter of American Women in Science (2012)
  • Louis and Artur Lucian Award for Research in Circulatory Diseases, McGill University (2010)
  • Scientific Accomplishment Award, American Thoracic Society (2008)
  • Distinguished Scientist Award, American Heart Association (2006)
  • Dickinson Richards Lecture, American Heart Association (2005)
  • Basic Research Prize, American Heart Association (2004)
View All 16honors and awards of Marlene Rabinovitch

Professional Education

Fellowship: Children's Hospital Harvard Medical School MA (1977)
Board Certification: Pediatrics, American Board of Pediatrics (1976)
Residency: University of Colorado Health Science Center CO (1973)
Board Certification: Pediatric Cardiology, American Board of Pediatrics (1979)
Internship: University of Colorado Health Science Center CO (1972)
Medical Education: McGill University, Canada (1971)
View All 8



Prior Year Coursescourses of Marlene Rabinovitch

Graduate and Fellowship Program Affiliations

Scientific Focus

Current Research and Scholarly Interests

Our research program seeks to identify the cellular and molecular programs regulating vascular and lung development. We then determine how these programs are perturbed by genetic abnormalities or injurious processes associated with disease. Our studies use high throughput genomic and microfluidic technologies, a variety of cell biology platforms including confocal and videomicroscopy, genetically modified mouse models of human disease, human tissue samples and induced pluripotent stem cells to answer these questions. Our major disease focus is pulmonary arterial hypertension (PAH), a condition that can be a fatal complication in children with heart defects, but also arises as a condition of unknown etiology primarily in young women. The pathological changes in the lung blood vessels that cause right-sided heart failure include loss of the distal microcirculation and obliterative proliferative changes occluding the lumen of larger arteries. Our goal is to learn how we can activate lung vascular developmental programs to regenerate lost microvessels and to reverse the obliterative changes. Over the past decade our research has led to four novel compounds in clinical trial or being positioned for clinical trial.

Our research projects have explored the link between the genetic mutation causing loss of function of bone morphogenetic protein receptor (BMPR) 2 and perturbation of Wingless (Wnt) signaling, PPARg mediated gene regulation, RNA translation, cross-talk with other cell surface receptors (PDGF, RAGE) and structural and functional derangement of the pulmonary circulation. We also address how viruses perturb microRNA function and how this might lead to the activation and production of neutrophil elastase in the vessel wall, and we use microfluidics to establish lung vascular and inflammatory cells that are transformed or abnormally expanded

NIH funded research uses induced pluripotent stem cells in collaboration with the laboratory of Dr. Joseph Wu and next generation sequencing in collaboration with the laboratory of Dr. Michael Snyder. Our team compares endothelial cells (ECs) derived from induced pluripotent stem cells (iPSC) with native ECs, to improve our understanding of pulmonary hypertension. Towards this goal, we are comparing gene variants (Exome/whole genome sequencing), epigenetic changes (DNA methylation, by Methyl-Seq) and RNA expression (by RNA-Seq) in iPSC-ECs derived from skin fibroblasts or blood cells,, iPSCs derived from pulmonary arterial EC, with native PAECs. from the same PAH patients or controls. Our second goal is to use iPSC-ECs derived from blood or skin of PAH patients to correct gene variants and to screen novel therapies to determine whether the EC functions of these cells normalize.

We have an NIH Translational Program Project with the laboratories of Drs. Richard Bland and Mark Nicolls to address the vulnerable microcirculation in pulmonary hypertension, chronic lung disease of prematurity and lung transplant rejection and to work toward translation of novel therapies including the elastase inhibitor elafin. Together with the Nolan, Robinson, Utz and Kodadek Groups on an NIH Proteomics Initiative we address autoimmunity and its relationship to the development of pulmonary hypertension. We use high throughput immunophenotyping and mass element flow cytometry (CYTOF) to identify abnormalities in the immune system and in the response to viral infection.

Other investigator-initiated research focuses on the pivotal role of PPARg as a transcription factor activated by BMPR2, and its novel role in DNA damage and repair.. These studies led to investigations linking p53, with PPARg and

Our research program harmonizes with that of Dr. Richard Bland who investigates the regulation, expression and function of genes that coordinate pulmonary alveolar and vascular development, and how they are perturbed by prematurity and mechanical ventilation, leading to chronic lung dis


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