Circulating Soluble TREM2 and Cardiovascular Outcome in Cohort Study of Coronary Atherosclerosis Patients
Autor: | Valeri Cuciuc, Sagi Tshori, Livi Grib, Gal Sella, Ortal Tuvali, Igor Volodarsky, Michael Welt, Michael Fassler, Sara Shimoni, Jacob George |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
Membrane Glycoproteins
Organic Chemistry Plaque Amyloid General Medicine Coronary Artery Disease Atherosclerosis Catalysis Computer Science Applications Inorganic Chemistry Cohort Studies Triggering Receptor Expressed in Myeloid Cells 2 sTREM2 atherosclerosis death inflammation ischemic heart disease Alzheimer Disease Humans Physical and Theoretical Chemistry Receptors Immunologic Molecular Biology Spectroscopy Biomarkers |
Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 21; Pages: 13121 |
ISSN: | 1422-0067 |
DOI: | 10.3390/ijms232113121 |
Popis: | Triggering Receptor Expressed in Myeloid Cells 2 (TREM2) is a membrane receptor in myeloid cells that mediates cellular phagocytosis and inflammation. TREM2 and its soluble extracellular domain are clearly implicated in neuroinflammation and neurodegeneration. sTREM2 is also expressed in atherosclerotic macrophages. We hypothesized that sTREM2 would predict cardiovascular mortality in patients with established coronary atherosclerosis (CAD). Consecutive patients undergoing coronary angiography with the establishment of the diagnosis of CAD (n = 230) and without CAD (n = 53) were tested for their baseline serum sTREM2 levels. All patients were followed up for 84 months or until death occurred. sTREM2 correlated with age; however, no association was found between sTREM2 and the number of atherosclerotic vessels involved (p = 0.642). After 84 months of follow-up, 68 out of the 230 CAD patients had died. After adjusting for age and other risk factors, the adjusted hazard ratio for the highest quartile of sTREM2 was 2.37 (95% confidence interval 1.17–4.83) for death. In patients with established CAD, serum sTREM2 appears to predict cardiovascular death as a potential surrogate for plaque rupture. TREM2 and its soluble extracellular form might be implicated in the fate of the atherosclerotic plaque, but corroboration within larger studies is needed. |
Databáze: | OpenAIRE |
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