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Expression correlation attenuates within and between key signaling pathways in chronic kidney disease
Hui Yu1, Danqian Chen2, Olufunmilola Oyebamiji1
1Department of Internal Medicine, University of New Mexico, Albuquerque, NM, 87131, USA.
BMC Medical Genomics
|September 22, 2020
Summary
Differential coexpression analysis revealed global correlation attenuation in chronic kidney disease (CKD) progression. This study identifies disrupted gene correlations and vanishing hub genes, offering insights into CKD's complex pathophysiological mechanisms.
Area of Science:
- Transcriptomics
- Systems Biology
- Bioinformatics
Background:
- Differential coexpression analysis offers a complementary view to differential expression in diseased transcriptomes.
- Previous studies observed global transcriptome correlation loss in aging and perturbed human subjects.
- Chronic kidney disease (CKD) lacks investigation into coexpression disruptions.
Purpose of the Study:
- To investigate coexpression disruptions in chronic kidney disease (CKD).
- To analyze transcriptome transitions from early to severe CKD phases using differential coexpression methods.
Main Methods:
- RNA-sequencing (RNA-seq) on kidney tissue from 140 CKD patients.
- Application of multiple differential coexpression analysis methods.
- Analysis of transcriptome changes across CKD stages.
Main Results:
- Global expression correlation attenuation observed during CKD progression.
- Regulation of nuclear SMAD2/3 signaling pathway showed significant intra-pathway correlation rewiring.
- Focal adhesion kinase signaling pathway exhibited weakened crosstalk with other pathways, including SMAD2/3 signaling.
- Genes like ACTN4 showed widespread correlation dissociation with partners across signaling pathways.
Conclusions:
- CKD progression is associated with global expression correlation attenuation within and between key signaling pathways.
- Identification of vanishing hub genes and disrupted correlations provides insights into CKD pathophysiology.
- The findings illuminate the molecular mechanisms underlying CKD progression.
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