Epithelial-mesenchymal interactions in pulmonary fibrosis.
Annu Rev Physiol
; 73: 413-35, 2011.
Article
em En
| MEDLINE
| ID: mdl-21054168
ABSTRACT
Lung epithelial cells have emerged as a frequent target of injury, a driver of normal repair, and a key element in the pathobiology of fibrotic lung diseases. An important aspect of epithelial cells is their capacity to respond to microenvironmental cues by undergoing epithelial-mesenchymal transition (EMT). EMT is not simply widespread conversion of epithelial cells to fibroblasts but a graded response whereby epithelial cells reversibly acquire mesenchymal features and enhanced capacity for mesenchymal cross-talk. Recent studies elucidate distinct integrin-sensing systems that coordinate activity of TGFß1, a critical signaling element regulating EMT, with the presence of proinflammatory signals and cell injury. Repeated injury superimposes persistent inflammation and hypoxia onto these highly regulated repair pathways, potentially overwhelming orderly repair and creating sustained fibrogenesis. Understanding specific signaling mechanisms driving the mesenchymal response to TGFß1 may reveal therapeutics to attenuate fibrogenesis yet preserve the important homeostatic functions of TGFß1.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fibrose Pulmonar
/
Transição Epitelial-Mesenquimal
Limite:
Animals
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
Annu Rev Physiol
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
Estados Unidos