Faculty Profile


Robert Guzy
Section of Pulmonary / Critical Care
Assistant Professor of Medicine
rguzy1@bsd.uchicago.edu
Referring Physician Access Line: 1-877-DOM-2730

Academic Interests

Dr. Guzy's research is focused on the mechanisms involved in recovery from lung injury, and how aberrant recovery from injury leads to fibroblast activation and the development of pulmonary fibrosis. The goal of his research is to understand the mechanisms regulating how lung epithelium, endothelium, and fibroblasts interact following injury to promote 1) repair following lung injury and ARDS and 2) pathological fibroblast proliferation resulting in a variety of lung diseases, including pulmonary fibrosis. His laboratory is interested in the cellular mechanisms by which growth Fibroblast Growth Factors (FGFs) and related pathways such as bone morphogenic protein (BMP) signaling are involved in lung injury and pulmonary fibrosis. Dr. Guzy studies the mechanism by which FGFs act as reparative agents following injury, and whether they can be utilized as therapeutic agents in lung injury and ARDS. He is also interested in how FGFs and BMP signaling interact with TGF-beta and other pro-fibrotic growth factors in fibroblasts in the setting of pulmonary fibrosis. Current work in his laboratory uses a combination of transgenic mouse models, animal models of lung injury and pulmonary fibrosis, and human translational studies.
 

Clinical Interests

Advanced Lung Diseases, Lung Transplantation, Interstitial Lung Diseases
 

Publications

  • Guzy RD, Stoilov I, Elton TJ, Mecham RP, Ornitz DM. 2015. FGF2 is required for epithelial recovery, but not for pulmonary fibrosis, in response to bleomycin. Am J Respir Cell Mol Biol. Jan;52(1):116-28
  • Kulkarni HS, Guzy RD, McEvoy C. YKL-40 in pediatric asthma, MUC5B promoter polymorphism in Idiopathic Pulmonary Fibrosis, and esmolol in septic shock. 2014. Am J Respir Crit Care Med. May 1;189(9):1138-40.
  • Guzy R.D., Sharma B., Bell E., Chandel N.S., Schumacker P.T. 2008. Loss of the SdhB, but not the SdhA, subunit of Complex II triggers reactive oxygen species-dependent hypoxia-inducible factor activation and tumorigenesis. Mol Cell Bio. Jan;28(2):718-31.
  • Guzy R.D., Mack M.M., Schumacker P.T. 2007 Mitochondrial Complex III is required for hypoxia-induced ROS production and gene transcription in yeast. Antioxid Redox Signal. Sep;9(9):1317-28.
  • Guzy R.D., Hoyos B., Robin E., Chen H., Liu L., Mansfield K.D., Simon M.C., Hammerling U., Schumacker P.T. 2005. Mitochondrial Complex III is required for hypoxia-induced ROS production and cellular oxygen sensing. Cell Metabolism Jun;1(6):401-408.
For a complete list of publications click here:

Training

  • PhD, 2005, The University of Chicago, Cellular Physiology
  • Fellowship, 2006, Northwestern University, Research - Cellular Physiology
  • MD, 2008, The University of Chicago,
  • Residency, 2010, Barnes-Jewish Hospital, Internal Medicine
  • Fellowship, 2014, Washington University, Pulmonary and Critical Care
  • Fellowship, 2015, Washington University, Research - Pulmonary and Critical Care