Journal
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
Volume 5, Issue -, Pages 77-98Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathol.4.110807.092217
Keywords
airway; asthma; emphysema; interstitial fibrosis
Categories
Funding
- National Institutes of Health [HL63993, PO1NS04415]
- Sandler Foundation
- American Lung-Association
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL063993] Funding Source: NIH RePORTER
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Fibrogenic lung reactions occur as a common phenotype shared among disorders of heterogeneous etiologies. Even with a common etiology, the extent and pattern of fibrosis vary greatly among individuals, even within families, suggesting complex gene-environment interactions. The search for mechanisms shared among all fibrotic lung diseases would represent a major advance in the identification of therapeutic targets that could have a broad impact on lung health. Although it is difficult to grasp all of the complexities of the varied cell types and cytokine networks involved in lung fibrogenic responses, and to predict the biologic responses to the overexpression or deficiency of individual cytokines, a large body of evidence converges on a single common theme: the central importance of the transforming growth factor beta (TGF-beta) pathway. Therapies that act upstream or downstream of TGF-beta activation have the therapeutic potential to treat all fibrogenic responses in the lung.
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