Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis.
Am J Physiol Lung Cell Mol Physiol
; 311(3): L590-601, 2016 Sep 01.
Article
in En
| MEDLINE
| ID: mdl-27474089
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by accumulation of extracellular matrix (ECM) and impaired gas exchange. The pathobiological mechanisms that account for disease progression are poorly understood but likely involve alterations in innate inflammatory cells, epithelial cells, and fibroblasts. Thus we seek to review the most recent literature highlighting the complex roles of neutrophils and macrophages as both promoters of fibrosis and defenders against infection. With respect to epithelial cells and fibroblasts, we review the data suggesting that defective autophagy promotes the fibrogenic potential of both cell types and discuss new evidence related to matrix metalloproteinases, growth factors, and cellular metabolism in the form of lactic acid generation that may have consequences for promoting fibrogenesis. We discuss potential cross talk between innate and structural cell types and also highlight literature that may help explain the limitations of current IPF therapies.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Autophagy
/
Idiopathic Pulmonary Fibrosis
/
Fibroblasts
/
Immunity, Innate
Type of study:
Etiology_studies
Limits:
Animals
/
Humans
Language:
En
Year:
2016
Type:
Article