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ABSTRACT: Background
Mouse models are useful for studying cigarette smoke (CS)-induced chronic pulmonary pathologies such as lung emphysema. To enhance translation of large-scale omics data from mechanistic studies into pathophysiological changes, we have developed computational tools based on reverse causal reasoning (RCR).Objective
In the present study we applied a systems biology approach leveraging RCR to identify molecular mechanistic explanations of pathophysiological changes associated with CS-induced lung emphysema in susceptible mice.Methods
The lung transcriptomes of five mouse models (C57BL/6, ApoE (-/-) , A/J, CD1, and Nrf2 (-/-) ) were analyzed following 5-7 months of CS exposure.Results
We predicted 39 molecular changes mostly related to inflammatory pro
SUBMITTER: Cabanski M
PROVIDER: S-EPMC4464601 | biostudies-literature | 2015 Jul
REPOSITORIES: biostudies-literature