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Updated: Aug 8, 2025

Dynamic Proteomic and miRNA Analysis of Polysomes from Isolated Mouse Heart After Langendorff Perfusion
Published on: August 29, 2018
Multi-omics integration to identify the genetic expression and protein signature of dilated and ischemic
Konstantina Portokallidou1,2, Nikolas Dovrolis1,2, Georgia Ragia1,2
1Laboratory of Pharmacology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece.
Insights
This study identified gene and protein signatures for dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM). These signatures reveal shared and distinct molecular pathways, offering potential diagnostic biomarkers and therapeutic targets for heart failure (HF).
Area of Science:
- Cardiology
- Genomics
- Proteomics
- Bioinformatics
Background:
- Heart failure (HF) is a major cause of morbidity.
- Dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) are key HF subtypes.
- Understanding their molecular signatures is crucial for targeted therapies.
Purpose of the Study:
- To identify distinct gene expression and protein signatures for DCM and ICM.
- To characterize the molecular pathways underlying these HF subtypes.
- To uncover potential diagnostic biomarkers and therapeutic targets for HF.
Main Methods:
- Utilized omics data from public repositories (GEO and PRIDE).
- Applied a multilayered bioinformatics approach to analyze transcriptomic and proteomic datasets.
- Performed enrichment analysis and constructed protein-protein interaction networks.
Main Results:
- Identified 10 differentially expressed genes/proteins in DCM (DiSig) and 15 in ICM (IsSig).
- Common pathways include extracellular matrix organization and cellular response to stress.
- Distinct pathways involve muscle tissue development (DCM) and immune cell activation (ICM).
Conclusions:
- The study provides molecular insights into HF etiopathology, highlighting similarities and differences between DCM and ICM.
- The identified DiSig and IsSig signatures offer cross-validated targets at both transcriptomic and proteomic levels.
- These signatures represent promising novel pharmacological targets and diagnostic biomarkers for HF.
Introduction:
Heart failure (HF) is a complex clinical syndrome leading to high morbidity. In this study, we aimed to identify the gene expression and protein signature of HF main causes, namely dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM).
Methods:
Omics data were accessed through GEO repository for transcriptomic and PRIDE repository for proteomic datasets. Sets of differentially expressed genes and proteins comprising DCM (DiSig) and ICM (IsSig) signatures were analyzed by a multilayered bioinformatics approach. Enrichment analysis via the Gene Ontology was performed through the Metascape platform to explore biological pathways. Protein-protein interaction networks were analyzed via STRING db and Network Analyst.
Results:
Intersection of transcriptomic and proteomic analysis showed 10 differentially expressed genes/proteins in DiSig (AEBP1, CA3, HBA2, HBB, HSPA2, MYH6, SERPINA3, SOD3, THBS4, UCHL1) and 15 differentially expressed genes/proteins in IsSig (AEBP1, APOA1, BGN, CA3, CFH, COL14A1, HBA2, HBB, HSPA2, LTBP2, LUM, MFAP4, SOD3, THBS4, UCHL1). Common and distinct biological pathways between DiSig and IsSig were retrieved, allowing for their molecular characterization. Extracellular matrix organization, cellular response to stress and transforming growth factor-beta were common between two subphenotypes. Muscle tissue development was dysregulated solely in DiSig, while immune cells activation and migration in IsSig.
Discussion:
Our bioinformatics approach sheds light on the molecular background of HF etiopathology showing molecular similarities as well as distinct expression differences between DCM and ICM. DiSig and IsSig encompass an array of "cross-validated" genes at both transcriptomic and proteomic level, which can serve as novel pharmacological targets and possible diagnostic biomarkers.
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Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy
Cardiomyopathy I: Introduction and Classification

