Figures
- Figure 1.
Schematic representation of the potential clinical courses of idiopathic pulmonary fibrosis. As disease progresses there is a subclinical period in which only radiographic findings of disease may be present, followed by a symptomatic period consisting of both pre- and post-diagnosis clinical phases. The rate of decline and progression to death may be rapid (A), slow (C and D) or mixed (B), with periods of relative stability interposed with periods of acute decline (#). Reproduced from [11] with permission.
- Figure 2.
A representation of the key factors controlling host–environment interactions and influencing individual phenotypes and, therefore, susceptibility to disease. Transcription of genes to RNA with translation to proteins is controlled by epigenetic modification and is subject to regulation by microRNAs. The role played by proteins (as receptors, growth factors and second messengers) is in turn influenced by a variety of post-translational modifications including glycosylation, citrullination and phosphorylation, all of which may be altered by disease (e.g. diabetes) or the environment (e.g. the host microbiome, pollution, cigarette smoke, etc.).
- Figure 3.
Developing a disease fingerprint. The combination of modern omic-based techniques together with careful longitudinal phenotyping of disease cohorts permits the development of a specific disease signature or fingerprint. Adopting such an approach should provide novel disease insights that inform understanding of disease biology and identification of therapeutic targets. Disease fingerprinting will also enable the development of diagnostic tools and should facilitate biomarker discovery, which in turn should improve early phase clinical trial design.
