Oxidative Inactivation of Cathepsin B in Idiopathic Pulmonary Fibrosis
Conference Year
January 2022
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by repeated micro injuries to the respiratory epithelium that result in altered repair pathways. Oxidative stress has long been associated with IPF pathogenesis, although the exact mechanisms that contribute to disease progression remain unclear. Protein s-glutathionylation (PSSG), a post-translational redox modification, has been demonstrated to increase in patients with IPF in conjunction with decreased activity of glutaredoxin-1 (GLRX), a key antioxidant enzyme responsible for its reversal. While the role of Glrx in fibrosis has been extensively studied, the S-glutathionylated protein targets that are impacted by Glrx inactivation remain under investigation.
Primary Faculty Mentor Name
Yvonne Janssen-Heininger
Secondary Mentor Name
Elizabeth Corteselli
Status
Undergraduate
Student College
College of Agriculture and Life Sciences
Program/Major
Microbiology
Primary Research Category
Biological Sciences
Oxidative Inactivation of Cathepsin B in Idiopathic Pulmonary Fibrosis
Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by repeated micro injuries to the respiratory epithelium that result in altered repair pathways. Oxidative stress has long been associated with IPF pathogenesis, although the exact mechanisms that contribute to disease progression remain unclear. Protein s-glutathionylation (PSSG), a post-translational redox modification, has been demonstrated to increase in patients with IPF in conjunction with decreased activity of glutaredoxin-1 (GLRX), a key antioxidant enzyme responsible for its reversal. While the role of Glrx in fibrosis has been extensively studied, the S-glutathionylated protein targets that are impacted by Glrx inactivation remain under investigation.