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Published on: April 30, 2020
Modular networks and genomic variation during progression from stable angina pectoris through ischemic cardiomyopathy
Lin Chen1,2, Ya-Nan Yu1, Jun Liu1
1Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, No. 16 Nanxiaojie, Dongzhimennei, Beijing, 100700, China.
Insights
This study reveals inflammation and angiogenesis link stable angina pectoris (SAP), ischemic cardiomyopathy (ICM), and chronic heart failure (CHF). Paired disease progression modules (PDPMs) identified these molecular relationships for better disease understanding.
Area of Science:
- Cardiovascular biology
- Systems biology
- Genomics
Background:
- Understanding disease-disease relationships is crucial for etiology, classification, and drug repositioning.
- The molecular connections among stable angina pectoris (SAP), ischemic cardiomyopathy (ICM), and chronic heart failure (CHF) remain unclear despite their causative links.
Purpose of the Study:
- To elucidate the molecular relationships among SAP, ICM, and CHF.
- To identify key molecular pathways and genomic variations linking these cardiovascular diseases.
Main Methods:
- Integrated multi-database data to construct paired disease progression modules (PDPMs).
- Employed K-value calculation for module reconstruction pairs (MRPs) to quantify disease relationships.
- Utilized enrichment analysis, literature validation, and structural variation (SV) analysis for verification.
Main Results:
- Identified 16 PDPMs among SAP, ICM, and CHF, with SAP-ICM showing the closest relationship.
- Inflammatory response pathways were common across SAP-ICM-CHF progression.
- Angiogenesis-related genes in the HIF-1 signaling pathway and specific structural variations (protein deletions/replications) were identified.
Conclusions:
- The PDPMs approach combined with genomic SV analysis offers a novel method for understanding disease progression.
- Inflammation and angiogenesis are highlighted as critical molecular links in the progression from SAP to ICM and CHF.
Background:
Analyzing disease-disease relationships plays an important role for understanding etiology, disease classification, and drug repositioning. However, as cardiovascular diseases with causative links, the molecular relationship among stable angina pectoris (SAP), ischemic cardiomyopathy (ICM) and chronic heart failure (CHF) is not clear.
Methods:
In this study, by integrating the multi-database data, we constructed paired disease progression modules (PDPMs) to identified relationship among SAP, ICM and CHF based on module reconstruction pairs (MRPs) of K-value calculation (a Euclidean distance optimization by integrating module topology parameters and their weights) methods. Finally, enrichment analysis, literature validation and structural variation (SV) were performed to verify the relationship between the three diseases in PDPMs.
Results:
Total 16 PDPMs were found with K > 0.3777 among SAP, ICM and CHF, in which 6 pairs in SAP-ICM, 5 pairs for both ICM-CHF and SAP-CHF. SAP-ICM was the most closely related by having the smallest average K-value (K = 0.3899) while the maximum is SAP-CHF (K = 0.4006). According to the function of the validation gene, inflammatory response were through each stage of SAP-ICM-CHF, while SAP-ICM was uniquely involved in fibrosis, and genes were related in affecting the upstream of PI3K-Akt signaling pathway. 4 of the 11 genes (FLT1, KDR, ANGPT2 and PGF) in SAP-ICM-CHF related to angiogenesis in HIF-1 signaling pathway. Furthermore, we identified 62.96% SVs were protein deletion in SAP-ICM-CHF, and 53.85% SVs were defined as protein replication in SAP-ICM, while ICM-CHF genes were mainly affected by protein deletion.
Conclusion:
The PDPMs analysis approach combined with genomic structural variation provides a new avenue for determining target associations contributing to disease progression and reveals that inflammation and angiogenesis may be important links among SAP, ICM and CHF progression.
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