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Single-Cell Multi-Omics Profiling of Immune Cells Isolated from Atherosclerotic Plaques in Male ApoE Knockout Mice Exposed to Arsenic.
Environ Health Perspect
January 2025
Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Canada.
Background: Millions worldwide are exposed to elevated levels of arsenic that significantly increase their risk of developing atherosclerosis, a pathology primarily driven by immune cells. While the impact of arsenic on immune cell populations in atherosclerotic plaques has been broadly characterized, cellular heterogeneity is a substantial barrier to in-depth examinations of the cellular dynamics for varying immune cell populations.
Objectives: This study aimed to conduct single-cell multi-omics profiling of atherosclerotic plaques in apolipoprotein E knockout () mice to elucidate transcriptomic and epigenetic changes in immune cells induced by arsenic exposure.
Adverse cardiovascular events are emerging with the use of immune checkpoint therapies in oncology. Using datasets in the Trans-Omics for Precision Medicine program (Multi-Ethnic Study of Atherosclerosis, Jackson Heart Study [JHS], and Framingham Heart Study), we examined the association of immune checkpoint plasma proteins with each other, their associated protein network with high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), and the association of HDL-C- and LDL-C-associated protein networks with all-cause mortality risk. Plasma levels of LAG3 and HAVCR2 showed statistically significant associations with mortality risk.
View Article and Find Full Text PDFCystine transporter SLC7A11 regulates sensitivity to unsaturated carbonyl compounds in mouse macrophage cell lines.
J Pharmacol Sci
February 2025
Department of Cellular Pharmacology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Nishi 7, Kita 15, Kita-ku, Sapporo, Hokkaido, 060-8638, Japan; Department of Neuropharmacology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Nishi 7, Kita 15, Kita-ku, Sapporo, Hokkaido, 060-8638, Japan.
Cytotoxic effects of cigarette smoke are thought to be causes of cigarette smoking-related diseases such as respiratory infection, chronic obstructive pulmonary disease, and atherosclerosis. Unsaturated carbonyl compounds are major cytotoxic factors in the gas phase of cigarette smoke. Cell death induced by unsaturated carbonyl compounds in cigarette smoke is PKC-dependent ferroptosis.
View Article and Find Full Text PDFEffects of LncRNA MYOSLID and MiR-29c-3p on the Proliferation and Migration of Angiotensin II-induced Vascular Smooth Muscle Cells.
Int Heart J
January 2025
Department of Cardiology, The Second Affiliated Hospital of Fujian Medical University.
Atherosclerosis (ATH) represents a major cause of cardiovascular disease. Long noncoding RNA (LncRNA) myocardin-induced smooth muscle lncRNA, inducer of differentiation (MYOSLID) and microRNA (miR) -29c-3p show substantial roles in ATH. We investigated their regulatory mechanisms on vascular smooth muscle cell (VSMC) proliferation and migration.
View Article and Find Full Text PDFCan fast wall shear stress computation predict adverse cardiac events in patients with intermediate non-flow limiting stenoses?
Atherosclerosis
December 2024
Department of Cardiology, Barts Heart Centre, Barts Health NHS Trust, London, UK; Centre for Cardiovascular Medicine and Devices, William Harvey Research Institute, Queen Mary University of London, London, UK. Electronic address:
Background And Aims: Coronary angiography-derived wall shear stress (WSS) may enable identification of vulnerable plaques and patients. A new recently introduced software allows seamless three-dimensional quantitative coronary angiography (3D-QCA) reconstruction and WSS computation within a single user-friendly platform carrying promise for clinical applications. This study examines for the first time the efficacy of this software in detecting vulnerable lesions in patients with intermediate non-flow limiting stenoses.
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