A computable cellular stress network model for non-diseased pulmonary and cardiovascular tissue.

ABSTRACT:

Background

Humans and other organisms are equipped with a set of responses that can prevent damage from exposure to a multitude of endogenous and environmental stressors. If these stress responses are overwhelmed, this can result in pathogenesis of diseases, which is reflected by an increased development of, e.g., pulmonary and cardiac diseases in humans exposed to chronic levels of environmental stress, including inhaled cigarette smoke (CS). Systems biology data sets (e.g., transcriptomics, phosphoproteomics, metabolomics) could enable comprehensive investigation of the biological impact of these stressors. However, detailed mechanistic networks are needed to determine which specific pathways are activated in response to different stressors and to drive the qualitative and eventu

SUBMITTER: Schlage WK 

PROVIDER: S-EPMC3224482 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature