Linked Life Data

17387717

Source:http://linkedlifedata.com/resource/pubmed/id/17387717

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-4-2
pubmed:abstractText
This review describes normal and abnormal wound healing, the latter characterized by excessive fibrosis and scarring, which for lung can result in morbidity and sometimes mortality. The cells, the extracellular matrix (ECM) proteins, and the growth factors regulating the synthesis, degradation, and deposition of the ECM proteins will be discussed. Therapeutics with particular emphasis given to gene therapies and their effects on specific signaling pathways are described. Bleomycin (BM), a potent antineoplastic antibiotic increases TGF-beta1 transcription, TGF-beta1 gene expression, and TGF-beta protein. Like TGF-beta1, BM acts through the same distal promoter cis-element of the COL1A1 gene causing increased COL1 synthesis and lung fibrosis. Lung fibroblasts exist as subpopulations with one subset predominantly responding to fibrogenic stimuli which could be a specific cell therapeutic target for the onset and development of pulmonary fibrosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
211
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
585-9
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Therapies for bleomycin induced lung fibrosis through regulation of TGF-beta1 induced collagen gene expression.
pubmed:affiliation
Department of Biochemistry, College of Medicine, 89 Beaumont Avenue, University of Vermont, Burlington, Vermont 05405, USA. kenneth.cutroneo@uvm.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural