Fibroproliferative disorders are the leading cause of morbidity and mortality
worldwide, with one specific group of fibroproliferative disorders being interstitial lung
diseases (ILD). Idiopathic pulmonary fibrosis is the most common ILD; however its
pathogenesis is not entirely understood. What is known is that there is repetitive cellular
injury preceding the fibrotic remodeling in the lungs that contributes to the irreversible
deposition of extracellular matrix (ECM) proteins. Myofibroblasts that accumulate at the
site of injury are thought to be the key drivers of ECM deposition and are often associated
in the disease. Although it is poorly understood how these immune cells differentiate in
the lung, one hypothesis suggests the role of alternatively activated profibrotic
macrophages in this process. The data presented in this thesis suggest that there are a presence of UPR and macrophage proteins in the lungs of IPF patients and the UPR may be necessary in the polarization of alternatively activated macrophages. / Thesis / Master of Science (MSc)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/22261 |
| Date | January 2017 |
| Creators | Tandon, Karun |
| Contributors | Ask, Kjetil, Medical Sciences |
| Source Sets | McMaster University |
| Language | English |
| Detected Language | English |
| Type | Thesis |
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