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Vinicio de Jesus Perez MD

Academic Appointments

Contact Information

  • Clinical Offices
    Pulmonary & Critical Care 300 Pasteur Dr H3142 MC 5236 Stanford, CA 94305
    Tel Work (650) 723-6381 Fax (650) 725-5489
  • Academic Offices
    Administrative Contact
    Michelle Fox Administrative Assistant Tel Work 1-650-723-5737
    Not for medical emergencies or patient use

Professional Snapshot

Clinical Focus

  • Pulmonary Disease
  • Pulmonary Hypertension

Administrative Appointments

  • Instructor, Stanford University (2006 - present)
  • Postdoctoral Research Fellow-Rabinovitch Lab, Stanford University (2004 - 2008)

Honors and Awards

  • Member-at-large, Cardiopulmonary, Critical Care, Perioperative & Resuscitation Council, American Heart Association (2010-)
  • Scholar, Harold Amos Career Development Award, Robert Wood Johnson Foundation (2010-2014)
  • ATS travel award, ATS (2009)
  • Finalist, BWF award, Burroughs Wellcome Fund (2009)
  • 2008 Professional of the year, Madison Who's who among pofessionals in America (2009)
View all 22honors and awards of Vinicio de Jesus Perez

Professional Education

Board Certification: Critical Care Medicine, American Board of Internal Medicine (2007)
Board Certification: Pulmonary Disease, American Board of Internal Medicine (2006)
Residency: Massachusetts General Hospital/Joslin Diabetes Center, MA (2003)
Internship: Massachusetts General Hospital/Joslin Diabetes Center, MA (2001)
Fellowship: Stanford University Medical Center, CA (2006)
View All 13

Graduate & Fellowship Program Affiliations

Scientific Focus

Research Interests

My research work is aimed at understanding how the following processes impact the development of abnormal vascular remodeling in Pulmonary Hypertension:

1) Role of the Wnt signaling pathways in regulation of pulmonary angiogenesis: I am currently working with both in vitro and murine transgenic models to determine whether abnotmalities in both canonical and noncanonical Wnt pathways may impact the function of BMP signaling in pulmonary endothelial cells and affect development of pulmonary hypertension.
2) Role of Wnt signaling in smooth muscle growth and movement: I am using both in vitro and a tissue specific conditional SM22 transgenic mouse to explore the impact of BMPRII knockdown on SMC behavior and explore the role that both canonical and noncanonical Wnt signaling pathways play in this response. In addition, we want to explore how the immediate extracellular environment may contribute to increase the susceptibility of SMC to surrounding growth factors and promote their unrestricted growth.
3) Role of BMPRI and II haploinsufficiency in PAH: Using a novel tamoxifen-CRE murine model, we will explore the contribution that dual reduction in expression of BMPRIa and II have on development of PAH. This work will also be complemented by use of genomic and molecular approaches to identify novel gene targets for future studies.

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