Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 211, Issue 3, Pages 585-589Publisher
WILEY-LISS
DOI: 10.1002/jcp.20972
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Funding
- NCRR NIH HHS [P20RR16435] Funding Source: Medline
- NHLBI NIH HHS [HL52285] Funding Source: Medline
- NIGMS NIH HHS [GM056581] Funding Source: Medline
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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 (EM), a potent antineoplastic antibiotic increases TGF-beta 1 transcription, TGF-beta 1 gene expression, and TGF-beta protein. Like TGF-beta 1, BM acts through the same distal promoter cis-element of the COL1A1 gene causing increased COIL1 synthesis and lung fibrosis. Lung fibroblasts exist as subpopulations with one subset predominately responding to fibrogenic stimuli which could be a specific cell therapeutic target for the onset and development of pulmonary fibrosis.
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