My career interests are focused on the interactions between TNF-α, macrophages and myofibroblasts and their role in the resolution of established pulmonary fibrosis with the goal to investigate the mechanisms by which TNF-α resolves fibrosis as the basis for the translational application of this work as a potential therapeutic. We plan to elucidate the mechanisms by which TNF-α is reducing the pro-fibrotic phenotype of macrophages and myofibroblasts and via the creation of an anti-fibrotic lung microenvironment. The importance of understanding how macrophages are shaping the lung environment during disease and how these interactions can be modulated to influence disease resolution is an important research direction that can be applied to many diseases including fibrosis and cancer. It is my goal that my basic science findings conducted in mouse models be translatable to human disease and into potential therapeutic treatments.
- University of Colorado Denver, PhD
Redente EF. How Do We Know What We Are Missing? Loss of Signaling through CD148 Drives Fibroblast Activation in Pulmonary Fibrosis. Am J Respir Crit Care Med. 2021 Aug 1;204(3):249-251. doi: 10.1164/rccm.202103-0737ED. PubMed PMID: 33891825; PubMed Central PMCID: PMC8513589.
Guzy R, Redente EF. Kindlin for the Fire: Targeting Proline Synthesis to Extinguish Matrix Production in Pulmonary Fibrosis. Am J Respir Cell Mol Biol. 2021 Jul;65(1):4-5. doi: 10.1165/rcmb.2021-0137ED. PubMed PMID: 33844940; PubMed Central PMCID: PMC8320124.
Associate Professor of the University of Colorado School of Medicine, Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine