Molecular Targets in Endovascular Progenitors to Inhibit Lung and Skin Fibrosis in Scleroderma
Abstract
Scleroderma and pulmonary fibrosis result from the development of fibrosis of undeterminedorigin. This proposal examines the vascular endothelium as a potential source of sclerodermafibrosis through a process called endothelial to mesenchymal transition (EndMT). It aimed toexplore EndMT as a potential mechanism of fibrosis in models of skin and pulmonary fibrosisreplicating scleroderma. It also tried to explore Sox9 as a potential target for therapy as it has beendescribed as a driver of EndMT in wound healing.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2022
- Accession Number
- AD1190400
Entities
People
- Kiarash Khosrotehrani
Organizations
- University of Queensland