Loss of SR-A and CD36 activity reduces atherosclerotic lesion complexity without abrogating foam cell formation in hyperlipidemic mice. - Wikidata - wikimedia - TriplyDB

Loss of SR-A and CD36 activity reduces atherosclerotic lesion complexity without abrogating foam cell formation in hyperlipidemic mice.

Loss of SR-A and CD36 activity reduces atherosclerotic lesion complexity without abrogating foam cell formation in hyperlipidemic mice.

http://www.wikidata.org/entity/Q37151524

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Diverse roles of macrophages in atherosclerosis: from inflammatory biology to biomarker discovery Fluid-phase pinocytosis of native low density lipoprotein promotes murine M-CSF differentiated macrophage foam cell formation Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis 11β-hydroxysteroid dehydrogenase type 1 gene knockout attenuates atherosclerosis and in vivo foam cell formation in hyperlipidemic apoE⁻/⁻ mice Macrophage sortilin promotes LDL uptake, foam cell formation, and atherosclerosis Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation Multimolecular signaling complexes enable Syk-mediated signaling of CD36 internalization Macrophages in the pathogenesis of atherosclerosis Macrophages create an acidic extracellular hydrolytic compartment to digest aggregated lipoproteins.Vav Guanine nucleotide exchange factors regulate atherosclerotic lesion development in mice.Receptor-independent fluid-phase pinocytosis mechanisms for induction of foam cell formation with native low-density lipoprotein particles Scavenger receptor structure and function in health and disease.Oxidized Lipoprotein Uptake Through the CD36 Receptor Activates the NLRP3 Inflammasome in Human Retinal Pigment Epithelial Cells.The impact of macrophage insulin resistance on advanced atherosclerotic plaque progression.CD36, a scavenger receptor involved in immunity, metabolism, angiogenesis, and behavior.Type 2 scavenger receptor CD36 in platelet activation: the role of hyperlipemia and oxidative stress.Induction of ER stress in macrophages of tuberculosis granulomas.Triglyceride Rich Lipoprotein -LPL-VLDL Receptor and Lp(a)-VLDL Receptor Pathways for Macrophage Foam Cell Formation.Macrophage death and defective inflammation resolution in atherosclerosis.CD36, a scavenger receptor implicated in atherosclerosis.Oxidized LDL: diversity, patterns of recognition, and pathophysiology.Large multiethnic Candidate Gene Study for C-reactive protein levels: identification of a novel association at CD36 in African Americans Identification and validation of genes affecting aortic lesions in mice Macrophage fatty-acid synthase deficiency decreases diet-induced atherosclerosis The role of endoplasmic reticulum stress in the progression of atherosclerosis.Internalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.Scavenger receptors and their potential as therapeutic targets in the treatment of cardiovascular disease Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure.Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress.Macrophages in atherosclerosis: a dynamic balance.Albumin-based microbubbles bind up-regulated scavenger receptors following vascular injury.A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulin signalling Inflammatory therapeutic targets in coronary atherosclerosis-from molecular biology to clinical application.OxLDL or TLR2-induced cytokine response is enhanced by oxLDL-independent novel domain on mouse CD36 Role of scavenger receptor A and CD36 in diet-induced nonalcoholic steatohepatitis in hyperlipidemic mice.Deficiency of PXR decreases atherosclerosis in apoE-deficient mice.The phosphoinositide 3-kinase signaling pathway is involved in the control of modified low-density lipoprotein uptake by human macrophages Murine bone marrow-derived macrophages differentiated with GM-CSF become foam cells by PI3Kγ-dependent fluid-phase pinocytosis of native LDL.LDL Receptor-Related Protein-1 (LRP1) Regulates Cholesterol Accumulation in Macrophages.

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P2860

Loss of SR-A and CD36 activity reduces atherosclerotic lesion complexity without abrogating foam cell formation in hyperlipidemic mice.

http://www.wikidata.org/entity/Q37151524

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 23 October 2008

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@en

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@nl

type

label

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@en

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@nl

prefLabel

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@en

Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@nl

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ATVBAHA.108.176644

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Arteriosclerosis, Thrombosis, and Vascular Biology

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Loss of SR-A and CD36 activity ...... mation in hyperlipidemic mice.

@en

P2093

Ira Tabas

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Jacqueline I Alvarez-Leite

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Jennifer J Manning-Tobin

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Maia Sharuk

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Mason W Freeman

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Menno P J de Winther

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Susan A Bell

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Tracie A Seimon

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P2860

Scavenger receptors class A-I/II and CD36 are the principal receptors responsible for the uptake of modified low density lipoprotein leading to lipid loading in macrophages

Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice

The response-to-retention hypothesis of early atherogenesis

Absence of CD36 protects against atherosclerosis in ApoE knock-out mice with no additional protection provided by absence of scavenger receptor A I/II

Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications

Response to Staphylococcus aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain

Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition

CD36 is a receptor for oxidized low density lipoprotein

Nonoxidative modifications of lipoproteins in atherogenesis.

Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice

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19-26

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scholarly article

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10.1161/ATVBAHA.108.176644

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1

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29

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Kathryn J Moore

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2008-10-23T00:00:00Z

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18948635

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atherosclerosis

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2666043

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