Pulmonary fibrosis is a phenotype that results from a variety of conditions and is associated with significant morbidity and mortality. Ongoing research in the field is driven by the need for effective treatments for pulmonary fibrosis. In this review, we highlight mechanisms that regulate gene expression in pulmonary fibrosis at multiple levels. Potential pathogenic mechanisms involve genetic background and transcriptional, posttranscriptional, translational, posttranslational, and epigenetic mechanisms. Pulmonary fibrosis results from abnormal gene expression and regulation that arise from a combination of inherited/acquired genetic alterations and environmental triggers. Collectively, these alterations result in increased expression of extracellular matrix components such as collagen and fibronectin and in the observed fibrosis. Insights gained from mechanisms identified to induce and/or perpetuate fibrosis in the lung will yield new targets for the development of more effective therapies.
|Number of pages||10|
|Journal||Critical Reviews in Eukaryotic Gene Expression|
|Publication status||Published - 01-01-2008|
All Science Journal Classification (ASJC) codes
- Molecular Biology