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Dysregulated Sheddase Signalling as a Molecular Driver of Plaque Instability Revealed by Integrative Transcriptomics.
Alaa G Alahmadi1, Hind A Alkhatabi1, Reem M Alotibi1
1Department of Biological Science, College of Science, University of Jeddah, Jeddah, Saudi Arabia.
Journal of Cellular and Molecular Medicine
|April 25, 2026
Summary
Investigating atherosclerotic plaques revealed significant differences in gene expression. Unstable plaques showed upregulation of pathways like sheddase and extracellular matrix degradation, suggesting new therapeutic targets for atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genomics
Background:
- Atherosclerosis is a leading cause of death driven by arterial inflammation and plaque remodeling.
- Understanding plaque biology and rupture mechanisms is crucial for managing atherosclerosis.
Purpose of the Study:
- To investigate transcriptomic differences between stable and unstable human carotid atherosclerotic plaques.
- To identify key molecular pathways associated with plaque instability using next-generation knowledge discovery (NGKD).
Main Methods:
- RNA sequencing data from stable and unstable plaque regions of four patients were analyzed.
- Differentially expressed genes (DEGs) were identified and analyzed using bioinformatics tools (WebGestalt, STRING DB, GSEA, IPA).
- Next-generation knowledge discovery (NGKD) methods were employed for pathway analysis.
Main Results:
- 4792 differentially expressed genes (DEGs) were identified in unstable plaques (p < 0.05).
- Upregulated pathways in unstable plaques included sheddase, collagen degradation, matrix metalloproteinase (MMP) activation, and extracellular matrix (ECM) degradation.
- Downregulated pathways included MMP inhibition and smooth muscle contraction.
Conclusions:
- The sheddase pathway is significantly upregulated in unstable atherosclerotic plaques.
- These findings highlight the sheddase pathway as a potential therapeutic target for atherosclerosis.
- Further research into ECM remodeling and MMPs in plaque instability is warranted.
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