Proteostasis signatures in human diseases
Fig 8
Proteostasis perturbations due to smoking are indicative of disease risk.
(A) Smokers present a higher similarity of proteostasis perturbations with at-risk diseases compared to reduced-risk diseases. Computing similarities of proteostasis proteins is more indicative of disease risk as compared to smoking-impacted kinases, transcription factors, or a random sample of differentially expressed genes. (B) At-risk diseases have a higher directional similarity of their perturbed proteostasis proteins with smoking. In contrast, reduced-risk diseases have a large proportion of perturbed proteostasis proteins that are deregulated in the opposite direction. (C) Genes encoding proteostasis proteins are perturbed similarly in smokers and patients with COPD. Genes similarly perturbed between smoking and COPD are likely to be contributive toward increasing COPD risk and onset. (D) Proteostasis proteins corresponding to genes perturbed in smokers and patients with PD. Proteostasis proteins oppositely perturbed between smoking and PD are likely to be protective against PD.