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SPA Promotes Atherosclerosis Through Mediating Macrophage Foam Cell Formation-Brief Report.
Arterioscler Thromb Vasc Biol
November 2024
Department of Surgery (S.D.K., D.C., M.M.F., S.-Y.C.), University of Missouri School of Medicine, Columbia.
Article Synopsis
- Atherosclerosis is an inflammatory disease where macrophage foam cells contribute significantly to its progression, and surfactant protein A (SPA) has not been previously studied in this context.
- Research showed that SPA expression is higher in atherosclerotic tissues, and its deficiency reduces cholesterol levels and foam cell formation in macrophages, leading to decreased atherosclerosis.
- SPA promotes atherosclerosis by enhancing the expression of scavenger receptor CD36, which plays a key role in cholesterol accumulation in macrophages.
Trem2 Agonist Reprograms Foamy Macrophages to Promote Atherosclerotic Plaque Stability-Brief Report.
Arterioscler Thromb Vasc Biol
July 2024
Center for Immunology (M.T.P., Y.X., H.H., V.O., P.R.S., A.E.K., F.B., A.Z., S.T., S.S., I.M.S., X.S.R., B.A.B., J.W.W.), University of Minnesota, Minneapolis.
Background: Trem2 (triggering receptor on myeloid cells 2), a surface lipid receptor, is expressed on foamy macrophages within atherosclerotic lesions and regulates cell survival, proliferation, and anti-inflammatory responses. Studies examining the role of Trem2 in atherosclerosis have shown that deletion of Trem2 leads to impaired foamy macrophage lipid uptake, proliferation, survival, and cholesterol efflux. Thus, we tested the hypothesis that administration of a Trem2 agonist antibody (AL002a) to atherogenic mice would enhance macrophage survival and decrease necrotic core formation to improve plaque stability.
View Article and Find Full Text PDFESR Essentials: imaging in stable chest pain - practice recommendations by ESCR.
Eur Radiol
October 2024
Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
Stable chest pain is a common symptom with multiple potential causes. Non-invasive imaging has an important role in diagnosis and guiding management through the assessment of coronary stenoses, atherosclerotic plaque, myocardial ischaemia or infarction, and cardiac function. Computed tomography (CT) provides the anatomical evaluation of coronary artery disease (CAD) with the assessment of stenosis, plaque type and plaque burden, with additional functional information available from CT fractional flow reserve (FFR) or CT myocardial perfusion imaging.
View Article and Find Full Text PDFSingle-Cell RNA Sequencing Reveals an Immune Landscape of CD4 T Cells in Coronary Culprit Plaques With Acute Coronary Syndrome in Humans-Brief Report.
Arterioscler Thromb Vasc Biol
May 2024
Division of Cardiovascular Medicine, Department of Internal Medicine (S.T., T.E., T. Yamashita, Y.S., T.H., H.O., K.-i.H.), Kobe University Graduate School of Medicine, Japan.
Background: Acute coronary syndrome (ACS) involves plaque-related thrombosis, causing primary ischemic cardiomyopathy or lethal arrhythmia. We previously demonstrated a unique immune landscape of myeloid cells in the culprit plaques causing ACS by using single-cell RNA sequencing. Here, we aimed to characterize T cells in a single-cell level, assess clonal expansion of T cells, and find a therapeutic target to prevent ACS.
View Article and Find Full Text PDFPrior Exposure to Experimental Preeclampsia Increases Atherosclerotic Plaque Inflammation in Atherogenic Mice-Brief Report.
Arterioscler Thromb Vasc Biol
April 2024
Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (L.A.B., J.J.M., N.D.C., B.V.C., I.Z.J.).
Background: Women with a history of preeclampsia have evidence of premature atherosclerosis and increased risk of myocardial infarction and stroke compared with women who had a normotensive pregnancy. Whether this is due to common risk factors or a direct impact of prior preeclampsia exposure has never been tested in a mouse atherosclerosis model.
Methods: Pregnant LDLR-KO (low-density lipoprotein receptor knockout; n=35) female mice were randomized in midgestation to sFlt1 (soluble fms-like tyrosine kinase 1)-expressing adenovirus or identical control adenovirus.
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