Office Address:
T-1218 MCN, MCN, Room / Suite T-1218, Nashville, TN 37232, Phone 615-936-0393

Assistant Professor of Medicine

Hometown
St. Louis, MO
Previous Institution
Vanderbilt University Medical Center
Previous Role/Title
Assistant Professor of Medicine
Specialty
Lung Transplantation, ARDS

Education

MD - Northwestern University Feinberg School of Medicine, 2007
PhD - Northwestern University Feinberg School of Medicine, 2005
BA - Biochemistry and Biology, Rice University, Houston, Texas

Postgraduate Training

Internship
Internship - Vanderbilt University Medical Center, 2008
Residency
Residency - Vanderbilt University Medical Center,  Chief Residency - Vanderbilt University Medical Center
Fellowship
Fellowship - Vanderbilt University Medical Center

Clinical Interest

Dr. Shaver subspecializes in the care of lung transplant recipients and patients with end stage lung disease who are seeking lung transplantation.
Research Keywords
acute respiratory distress syndrome, acute lung injury, cell-free hemoglobin, macrophage, lung transplantation, primary graft dysfunction
Research Description
Dr. Ciara Shaver is an Assistant Professor of Medicine at Vanderbilt University Medical Center in the Division of Allergy, Pulmonary, and Critical Care Medicine. Her growing basic and translational research program centers on mechanisms of acute lung injury with an emphasis on inflammation during critical illness and after lung transplantation. Several years ago, we discovered that elevated levels of cell-free hemoglobin were present in the airspace during ARDS and in the circulation prior to lung transplantation. Current research in my laboratory is focused on discovery of the pathways and cell types required for cell-free hemoglobin induced lung injury using a variety of in vitro and in vivo model systems. A second focus of my research is the mechanisms of primary graft dysfunction after lung transplantation. We recently discovered that circulating levels of cell-free hemoglobin prior to lung transplant are independently associated with increased risk of primary graft dysfunction. Using an ex vivo human lung perfusion model, we demonstrated that hemoglobin directly injures the lung endothelium and identified a potential therapy that may mitigate hemoglobin-mediated lung injury. In the future, my laboratory will continue to use murine and human lung model systems to comprehensively explore the underlying mechanisms of ARDS and primary graft dysfunction. I also manage a biorepository including explanted human lungs, declined human donor lungs, and serial bronchoalveolar lavage, blood, and biopsy samples from lung transplant recipients to facilitate detailed basic and translational studies in a variety of acute and chronic lung illnesses.