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COMP (Cartilage Oligomeric Matrix Protein) Neoepitope: A Novel Biomarker to Identify Symptomatic Carotid Stenosis
Open accessAbstract
Objective: COMP (cartilage oligomeric matrix protein) is abundantly expressed in the cardiovascular system, cartilage, and atherosclerotic plaques. We investigated if the total COMP (COMPtotal) and COMP neoepitope (COMPneo) with other cardiovascular markers and clinical parameters could identify symptomatic carotid stenosis. Approach and Results: Blood samples were collected from patients with symptomatic carotid stenosis (stenosis, n=50), patients with stroke without carotid stenosis but small plaques (plaque, n=50), and control subjects (n=50). COMPtotal and COMPneo were measured using an ELISA. Ninety-two cardiovascular disease markers were measured by the Olink CVD kit. The presence of native COMP and COMPneo was determined by immunohistochemistry. The concentration of COMPneo was higher and COMPtotal was lower in the stenosis group. When the concentration was compared between the stenosis and control groups, IL-1ra (interleukin-1 receptor antagonist protein), IL6 (interleukin-6), REN (Renin), MMP1 (matrix metalloproteinase-1), TRAIL-R2 (tumor necrosis factor-related apoptosis-inducing ligand receptor 2), ITGB1BP2 (integrin beta 1 binding protein 2), and COMPneo were predictive of stenosis. Conversely, KLK6 (kallikrein-6), COMPtotal, NEMO (nuclear factor-kappa-B essential modulator), SRC (Proto-oncogene tyrosine-protein kinase Src), SIRT2 (SIR2-like protein), CD40 (cluster of differentiation 40), TF (tissue factor), MP (myoglobin), and RAGE (receptor for advanced glycation end-products) were predictive of the control group. Model reproducibility was good with the receiver operating characteristic plot area under the curve being 0.86. When comparing the plaque group and stenosis group, COMPneo, GAL (galanin), and PTX3 (pentraxin-related protein PTX3) were predictive of stenosis. Model reproducibility was excellent (receiver operating characteristic plot area under the curve 0.92). COMPneo was detected in smooth muscle-, endothelial-, and foam-cells in carotid stenosis. Conclusions: Degradation of COMP may be associated with atherosclerosis progression and generation of a specific COMP fragment—COMPneo. This may represent a novel biomarker that together with COMPtotal and other risk-markers could be used to identify symptomatic carotid stenosis. Graphic Abstract: A graphic abstract is available for this article.
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Sandstedt et al. showed that while COMP expression is upregulated in human carotid plaques, decreased levels of COMP in plasma likely result from its degradation in severe atherosclerosis, leading to release of specific fragments (COMPneo) into bloodstream and reduced intact COMP detectable in plasma.
“They showed that while COMP expression is upregulated in human carotid plaques, decreased levels of COMP in plasma likely result from its degradation in severe atherosclerosis, leading to the release of specific fragments (COMPneo) into the bloodstream and reduced intact COMP detectable in plasma.”
From Aortic valve-specific genes dysregulated in calcific aortic valve stenosis as potential biomarkers and therapeutic targets (2025) · cites this paper as [56]
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Experimental — accuracy not yet measuredThe observed discrepancy between COMP valve mRNA and plasma protein level in CAVS could be attributed to the degradation of COMP within diseased aortic valve tissues.
“The observed discrepancy between COMP valve mRNA and plasma protein level in CAVS could be attributed to the degradation of COMP within diseased aortic valve tissues.”
From Aortic valve-specific genes dysregulated in calcific aortic valve stenosis as potential biomarkers and therapeutic targets (2025) · cites this paper as [56]
The Results and Discussion (page not provided) report lower plasma COMPtotal and evidence of COMP degradation in patients with carotid stenosis. They do not examine diseased aortic valves, CAVS, or valve COMP mRNA, so they cannot establish that degradation explains the claimed mRNA–plasma protein discrepancy. (LLM, conf=0.86)
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Cartilage Oligomeric Matrix Protein, Diseases, and Therapeutic Opportunities
Cui, J., & Zhang, J. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169253 · Cited by 77
Zamani, P., Houessou, U., Manikpurage, H. D., Li, Z., Dahmene, M., Gaudreault, N., Dagenais, F., Clavel, M.-A., Pibarot, P., Arsenault, B. J., et al. (2025) · Human Genetics and Genomics Advances · doi:10.1016/j.xhgg.2025.100448 · Cited by 3
Metadata
- Authors
- Sandstedt, J., Vargmar, K., Björkman, K., Ruetschi, U., Bergström, G., Hultén, L. M., & Skiöldebrand, E.
- Affiliations
- Sahlgrenska University Hospital (SE)
- Swedish University of Agricultural Sciences (SE)
- Department of Laboratory Medicine, Institute of Biomedicine (J.S., U.R.), Sahlgrenska Academy, University of Gothenburg, Sweden.
- University of Gothenburg (SE)
- Corresponding author
- Skiöldebrand, Eva
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2021-03
- Volume
- 41
- Issue
- 3
- Pages
- 1218-1228
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC7901532
- OpenAlex
- W3122847810
- Cited by
- 15
- References
- 1
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 3 · 2021: 1
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Epsilon Open Archive (Sveriges lantbruksuniversitet biblioteket (Swedish University of Agricultural Sciences)) (submittedVersion)
- Funders
- Hjärt-Lungfonden
- Vetenskapsrådet
- Sahlgrenska Universitetssjukhuset
- Svenska Läkaresällskapet
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cerebrovascular and Carotid Artery Diseases
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Keywords
- cartilage oligomeric matrix protein, symptomatic carotid stenosis, atherosclerosis, cardiovascular biomarkers, stroke, atherosclerotic plaque, smooth muscle cells, foam cells, endothelial cells, pentraxin 3, interleukin-1 receptor antagonist, interleukin-6, MMP-1, DR5
- MeSH terms
- Proto-Oncogene Mas, Aged, Epitopes, Female, Humans, Male, Middle Aged, Models, Cardiovascular, Biomarkers, Case-Control Studies, Carotid Stenosis, Disease Progression, Stroke, Plaque, Atherosclerotic, Cartilage Oligomeric Matrix Protein
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