Sanjeev Datar, MD, PhD
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
- HIF-1a promotes cellular growth in lymphatic endothelial cells exposed to chronically elevated pulmonary lymph flow.
- Mechanical forces alter endothelin-1 signaling: comparative ovine models of congenital heart disease.
- Mechanical Forces Alter Endothelin-1 Signaling: Comparative Ovine Models of Congenital Heart Disease.
- The Adaptive Right Ventricle in Eisenmenger Syndrome: Potential Therapeutic Targets for Pulmonary Hypertension?.
- Ovine Models of Congenital Heart Disease and the Consequences of Hemodynamic Alterations for Pulmonary Artery Remodeling.
- Correction: Preservation of myocardial contractility during acute hypoxia with OMX-CV, a novel oxygen delivery biotherapeutic.
- Preservation of myocardial contractility during acute hypoxia with OMX-CV, a novel oxygen delivery biotherapeutic.
- Analysis of the microRNA signature driving adaptive right ventricular hypertrophy in an ovine model of congenital heart disease.
- Lymphatic dysfunction in critical illness.
- KLF2-mediated disruption of PPAR-? signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow.
- Altered Carnitine Homeostasis in Children With Increased Pulmonary Blood Flow Due to Ventricular Septal Defects.
- Pulmonary artery smooth muscle cell hyperproliferation and metabolic shift triggered by pulmonary overcirculation.
- Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow.
- Right ventricular nitric oxide signaling in an ovine model of congenital heart disease: a preserved fetal phenotype.
- Sox18 preserves the pulmonary endothelial barrier under conditions of increased shear stress.
- Adaptive right ventricular performance in response to acutely increased afterload in a lamb model of congenital heart disease: evidence for enhanced Anrep effect.
- Altered reactivity and nitric oxide signaling in the isolated thoracic duct from an ovine model of congenital heart disease with increased pulmonary blood flow.
- Pulmonary Hypertension.
- Preoperative B-type natriuretic peptide levels are associated with outcome after total cavopulmonary connection (Fontan).
- L-carnitine preserves endothelial function in a lamb model of increased pulmonary blood flow.
- 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).
- Tezosentan increases nitric oxide signaling via enhanced hydrogen peroxide generation in lambs with surgically induced acute increases in pulmonary blood flow.
- Chronic inhibition of PPAR-? signaling induces endothelial dysfunction in the juvenile lamb.
- Rosiglitazone preserves pulmonary vascular function in lambs with increased pulmonary blood flow.
- Endostatin, an inhibitor of angiogenesis, decreases after bidirectional superior cavopulmonary anastamosis.
- PPAR-? regulates carnitine homeostasis and mitochondrial function in a lamb model of increased pulmonary blood flow.
- B-type natriuretic peptide levels predict outcomes in infants undergoing cardiac surgery in a lesion-dependent fashion.
- Pulmonary interstitial glycogenosis: an unrecognized etiology of persistent pulmonary hypertension of the newborn in congenital heart disease?
- B-Type Natriuretic Peptide (BNP) in Neonates, Infants and Children Undergoing Cardiac Surgery.
- Altered lymphatics in an ovine model of congenital heart disease with increased pulmonary blood flow.
- Attenuated vasodilatation in lambs with endogenous and exogenous activation of cGMP signaling: role of protein kinase G nitration.
- Advances in the management of pediatric pulmonary hypertension.
- Pediatric pulmonary arterial hypertension: current and emerging therapeutic options.
- Delineating the angiogenic gene expression profile before pulmonary vascular remodeling in a lamb model of congenital heart disease.
- Nitric oxide alterations following acute ductal constriction in the fetal lamb: a role for superoxide.
- Alterations in lung arginine metabolism in lambs with pulmonary hypertension associated with increased pulmonary blood flow.
- A CAUSAL DESIGN TRAJECTORY LINKS DIVERSE FORMS OF PULMONARY HYPERTENSION: EVIDENCE OF A FETAL PHENOTYPE OF ARTERIAL REMODELING UNDER THE PRINCIPLE OF MINIMUM WORK.
- Progressive dysfunction of nitric oxide synthase in a lamb model of chronically increased pulmonary blood flow: a role for oxidative stress.
- Mammalian cyclin D1/Cdk4 complexes induce cell growth in Drosophila.
- Drosophila Cdk4 is required for normal growth and is dispensable for cell cycle progression.
- The Drosophila cyclin D-Cdk4 complex promotes cellular growth.
- Zygotic degradation of two maternal Cdc25 mRNAs terminates Drosophila's early cell cycle program.