English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Tissue remodeling is a common pathology in many diseases. The reparative processes of wound healing result in an increase in extracellular matrix (ECM) generation, serving to restore barrier protection and normal tissue architecture. However in the lung, increased formation of ECM results in decreased lung compliance and impaired gas exchange. The chronic lung diseases COPD (chronic obstructive pulmonary disease) and IPF (idiopathic pulmonary fibrosis) both exhibit increased extracellular matrix (ECM) deposition within the lung due to increased stromal cell number and activation. The chronic nature of the disease is hypothesized to correlate with the extent of scarring and remodeling, with greater evidence being available for COPD rather than IPF. The potential underlying causes of both diseases are numerous, including direct insults to the lung such as cigarette smoke or exhaust particles; as well as underlying autoimmune conditions such as scleroderma or collagen vascular disease. Moreover, a correlation between COPD and smoking is well established; however, any causes for IPF, apart from a familial link, are currently not understood. To date there are no approved anti-fibrotic therapies that target the underlying remodeling in either disease. In order to treat this pathology, understanding the mechanisms promoting continual ECM deposition may elucidate novel therapeutic approaches that could provide clinical benefit to patients suffering from these debilitating diseases. This Chapter will focus on the cellular mechanisms and interactions within the fibrotic lung including resident fibroblast-epithelial cells as well as the cross-talk between fibroblasts and recruited bone marrow derived cells such as fibrocytes and monocytes. Also, the soluble mediators that have been associated with disease and how these can directly and indirectly modulate stromal cell activation will be discussed.

Mechanisms Promoting Chronic Lung Diseases: Will Targeting Stromal Cells Cure COPD and IPF?