This implies shared pathways which can result in toxic symptoms especially in an excess of metal.
As a result, 33 unique pathways were obtained from the shared pathways by GWAS datasets or PBA tools.
In addition, these networks can be constructed based on shared pathways [35], shared miRNA [36], shared protein complex [37], shared disease ontology [38] and disease comorbidity [39].
We also note that a disease similarity network can be constructed based on shared disease gene [30], shared pathways [35], shared miRNA [36], shared protein complex [37], shared disease ontology [38] and disease comorbidity [39].
Using this method, 17 shared pathways and 5 specific pathways were found to be significantly differentially expressed following infection with the two iridoviruses, among which 11 pathways were additionally identified based on the proposed method of multiple reference species selection.
Here, we review the current evidence for this shared genetic architecture and, based on these data, outline models for shared pathways, the underlying hypotheses for them, how these models can be tested and validated.
Candidate shared pathways include changes in hormonal milieu, inflammation, oxidative stress, DNA damage and compromised DNA repair, genetic susceptibility, decreased brain blood flow or disruption of the blood-brain barrier, direct neurotoxicity, decreased telomere length, and cell senescence.
Based on this observation, we set out to investigate disease relationships based on their shared pathways.
The combined p-values were calculated for the shared pathways among diseases using Fisher's method [40].
Finally, we ranked the associations among diseases based on the statistical significance of shared pathways in each database (Table S6).
Gene network analysis based on gene profiling data may represent a powerful method to predict key gene regulators and identify shared pathways among distinct categories of complex diseases.
