Inhibition of MEK and PI3K alone or in combination alters the transcriptome of the lung during TGF?-induced pulmonary fibrosis

ABSTRACT: Pulmonary fibrosis is often triggered by an epithelial injury resulting in the formation of fibrotic lesions in the lung, which progress to impair gas exchange and ultimately cause death. Recent clinical trials using drugs that target either inflammation or a specific molecule have failed, suggesting that multiple pathways and cellular processes need to be attenuated for effective reversal of established and progressive fibrosis. Although activation of MAPK and PI3K pathways have been detected in human fibrotic lung samples, the therapeutic benefits of in vivo modulation of the MAPK and PI3K pathways in combination are unknown. Overexpression of TGF? in the lung epithelium of transgenic mice results in the formation of fibrotic lesions similar to those found in human pulmonary fibrosis, an

ORGANISM(S): Mus musculus

SUBMITTER: Jing Chen 

PROVIDER: E-GEOD-52854 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress