Linked Life Data

21054168

Source:http://linkedlifedata.com/resource/pubmed/id/21054168

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-2-14
pubmed:abstractText
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 TGF?1, 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 TGF?1 may reveal therapeutics to attenuate fibrogenesis yet preserve the important homeostatic functions of TGF?1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1545-1585
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-35
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Epithelial-mesenchymal interactions in pulmonary fibrosis.
pubmed:affiliation
Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, 94143, USA. hal.chapman@ucsf.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural