Sanjeev Datar, MD, PhD

Education
2019 - Diversity, Equity, and Inclusion Champion Training, University of California
Fellowship, Pediatric Critical Care Medicine, 2008 - School of Medicine, University of California, San Francisco
Residency, Pediatrics, 2004 - School of Medicine, University of California, San Francisco
M.D., 2001 - School of Medicine, University of Washington
Ph.D., 2000 - Molecular and Cellular Biology, University of Washington/Fred Hutchinson Cancer Research Center
B.S., 1991 - Molecular Biophysics & Biochemistry, Yale University
Honors and Awards
  • RAP Pilot Grant for Established Investigators, UCSF, 2022
  • Pediatric Heart Center Catalyst Award, UCSF Benioff Children's Hospitals, 2022
  • RAP Pilot Grant for Junior Investigators, UCSF, 2014
  • Elected as Member of the Society for Pediatric Research, Council of the Society for Pediatric Research, 2013
  • Ida M. Cannon Award: The Dorothy Bradley Award for Integrity, The Pediatric Social Work Department, UCSF Benioff Children's Hospital, 2013
  • WSA Beginning Grant-in-Aid Award, American Heart Association, 2012
  • Excellence in Teaching Award, The Haile T. Debas Academy of Medical Educators, 2012
  • Charlotte Coleman Frey Pediatric Intensive Care Fellowship Award, Children's Hospital & Research Center Oakland, 2007
  • ACE Partnership Award, Science and Health Education Partnership, 2003
  • ARCS Foundation Fellow, Achievement Rewards for College Scientists (ARCS), 1998
  • Fred Hutchinson Scholarship Award for Outstanding Scholarship in the Field of Cancer Research, Fred Hutchinson Cancer Research Center, 1995
  • MSTP Fellow, University of Washington, 1992-2000
Websites
Publications
  1. HIF-1a promotes cellular growth in lymphatic endothelial cells exposed to chronically elevated pulmonary lymph flow.
  2. Mechanical forces alter endothelin-1 signaling: comparative ovine models of congenital heart disease.
  3. Mechanical Forces Alter Endothelin-1 Signaling: Comparative Ovine Models of Congenital Heart Disease.
  4. The Adaptive Right Ventricle in Eisenmenger Syndrome: Potential Therapeutic Targets for Pulmonary Hypertension?.
  5. Ovine Models of Congenital Heart Disease and the Consequences of Hemodynamic Alterations for Pulmonary Artery Remodeling.
  6. Correction: Preservation of myocardial contractility during acute hypoxia with OMX-CV, a novel oxygen delivery biotherapeutic.
  7. Preservation of myocardial contractility during acute hypoxia with OMX-CV, a novel oxygen delivery biotherapeutic.
  8. Analysis of the microRNA signature driving adaptive right ventricular hypertrophy in an ovine model of congenital heart disease.
  9. Lymphatic dysfunction in critical illness.
  10. KLF2-mediated disruption of PPAR-? signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow.
  11. Altered Carnitine Homeostasis in Children With Increased Pulmonary Blood Flow Due to Ventricular Septal Defects.
  12. Pulmonary artery smooth muscle cell hyperproliferation and metabolic shift triggered by pulmonary overcirculation.
  13. Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow.
  14. Right ventricular nitric oxide signaling in an ovine model of congenital heart disease: a preserved fetal phenotype.
  15. 162.
  16. 220.
  17. Sox18 preserves the pulmonary endothelial barrier under conditions of increased shear stress.
  18. Adaptive right ventricular performance in response to acutely increased afterload in a lamb model of congenital heart disease: evidence for enhanced Anrep effect.
  19. Altered reactivity and nitric oxide signaling in the isolated thoracic duct from an ovine model of congenital heart disease with increased pulmonary blood flow.
  20. Pulmonary Hypertension.
  21. Preoperative B-type natriuretic peptide levels are associated with outcome after total cavopulmonary connection (Fontan).
  22. L-carnitine preserves endothelial function in a lamb model of increased pulmonary blood flow.
  23. The effect of preoperative nutritional status on postoperative outcomes in children undergoing surgery for congenital heart defects in San Francisco (UCSF) and Guatemala City (UNICAR).
  24. Tezosentan increases nitric oxide signaling via enhanced hydrogen peroxide generation in lambs with surgically induced acute increases in pulmonary blood flow.
  25. Chronic inhibition of PPAR-? signaling induces endothelial dysfunction in the juvenile lamb.
  26. Rosiglitazone preserves pulmonary vascular function in lambs with increased pulmonary blood flow.
  27. Endostatin, an inhibitor of angiogenesis, decreases after bidirectional superior cavopulmonary anastamosis.
  28. PPAR-? regulates carnitine homeostasis and mitochondrial function in a lamb model of increased pulmonary blood flow.
  29. B-type natriuretic peptide levels predict outcomes in infants undergoing cardiac surgery in a lesion-dependent fashion.
  30. Pulmonary interstitial glycogenosis: an unrecognized etiology of persistent pulmonary hypertension of the newborn in congenital heart disease?
  31. B-Type Natriuretic Peptide (BNP) in Neonates, Infants and Children Undergoing Cardiac Surgery.
  32. Altered lymphatics in an ovine model of congenital heart disease with increased pulmonary blood flow.
  33. Attenuated vasodilatation in lambs with endogenous and exogenous activation of cGMP signaling: role of protein kinase G nitration.
  34. Advances in the management of pediatric pulmonary hypertension.
  35. Pediatric pulmonary arterial hypertension: current and emerging therapeutic options.
  36. Delineating the angiogenic gene expression profile before pulmonary vascular remodeling in a lamb model of congenital heart disease.
  37. Nitric oxide alterations following acute ductal constriction in the fetal lamb: a role for superoxide.
  38. Alterations in lung arginine metabolism in lambs with pulmonary hypertension associated with increased pulmonary blood flow.
  39. A CAUSAL DESIGN TRAJECTORY LINKS DIVERSE FORMS OF PULMONARY HYPERTENSION: EVIDENCE OF A FETAL PHENOTYPE OF ARTERIAL REMODELING UNDER THE PRINCIPLE OF MINIMUM WORK.
  40. Progressive dysfunction of nitric oxide synthase in a lamb model of chronically increased pulmonary blood flow: a role for oxidative stress.
  41. Mammalian cyclin D1/Cdk4 complexes induce cell growth in Drosophila.
  42. Drosophila Cdk4 is required for normal growth and is dispensable for cell cycle progression.
  43. The Drosophila cyclin D-Cdk4 complex promotes cellular growth.
  44. Zygotic degradation of two maternal Cdc25 mRNAs terminates Drosophila's early cell cycle program.