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Immuno-Metabolic Reprogramming in Metabolic Syndrome and Its Cardiovascular Complications: An Integrative
Komal Shrivastav1,2, Sushama Jadhav3, Pratik Mahajan4
1ICMR-National Institute for Tribal Health Research (NITHR), Jabalpur 482003, India.
International Journal of Molecular Sciences
|July 15, 2026
Summary
Metabolic syndrome and diabetic coronary artery disease share immune-inflammatory pathways. Key genes like CD86 and CD33, and miRNAs, may be therapeutic targets for these conditions.
Area of Science:
- Cardiovascular Science
- Immunology
- Genomics
Background:
- Metabolic syndrome (MeS) is a significant risk factor for cardiovascular disease, involving inflammation and metabolic issues.
- The molecular links between MeS and diabetic coronary artery disease (DMCAD) are not fully understood.
Purpose of the Study:
- To elucidate the molecular mechanisms connecting MeS to DMCAD using bioinformatics.
- To identify potential biomarkers and therapeutic targets for inflammation-driven cardiometabolic diseases.
Main Methods:
- Analysis of peripheral blood mononuclear cell transcriptomic data from MeS and DMCAD patients.
- Utilized differential gene expression, pathway enrichment, protein-protein interaction networks, WGCNA, GSEA, and miRNA regulatory network analysis.
- Validated candidate genes using an independent type 2 diabetes mellitus dataset.
Main Results:
- Identified immune-inflammatory and immuno-metabolic pathways as central to both MeS and DMCAD.
- Highlighted key hub genes (CD86, CD33, CCR1, C5AR1, FPR1, CXCL16, LILRA5) involved in immune regulation and cardiometabolic dysfunction.
- Identified miR-17/92 family and miR-146a-5p as potential upstream regulators, linked to inflammation and angiogenesis.
Conclusions:
- Coordinated immune-inflammatory and metabolic signaling networks drive the progression from MeS to DMCAD.
- Identified hub genes and miRNAs represent potential biomarkers and therapeutic targets for inflammation-driven cardiometabolic diseases.
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