Multiple inflammatory markers in patients with significant coronary artery disease

Videm, Vibeke; Wiseth, Rune; Gunnes, Sigurd; Madsen, Hans O.; Garred, Peter

doi:10.1016/j.ijcard.2006.07.005

Cited by 40 publications

(45 citation statements)

References 23 publications

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“…The sequestration of neutrophils into the peritoneal cavity is thus most likely a protective response induced by the accumulation of heavily lipid-laden peritoneal macrophages in absence of both SR-BI and ABCA1. Interestingly, neutrophil activation is increased in patients with significant coronary stenosis, 45 and enhanced neutrophil infiltration is observed in culprit lesions in acute coronary syndromes, 46 suggesting an important role for neutrophils in atherosclerosis. In agreement, neutrophil depletion reduces atherosclerotic lesion development in apoE KO mice.…”

Section: E28mentioning

confidence: 99%

Enhanced Foam Cell Formation, Atherosclerotic Lesion Development, and Inflammation by Combined Deletion of ABCA1 and SR-BI in Bone Marrow–Derived Cells in LDL Receptor Knockout Mice on Western-Type Diet

Zhao

Pennings

Hildebrand

et al. 2010

Circulation Research

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Rationale: Macrophages cannot limit the uptake of lipids and rely on cholesterol efflux mechanisms for maintaining cellular cholesterol homeostasis. Important mediators of macrophage cholesterol efflux are ATP-binding cassette transporter 1 (ABCA1), which mediates the efflux of cholesterol to lipid-poor apolipoprotein AI, and scavenger receptor class B type I (SR-BI), which promotes efflux to mature high-density lipoprotein. Objective:The aim of the present study was to increase the insight into the putative synergistic roles of ABCA1 and SR-BI in foam cell formation and atherosclerosis. ABCA1 is a full-size ABC-transporter that facilitates cholesterol efflux to lipid-poor apolipoprotein (apo)AI. 2,3 Totalbody ABCA1 knockout mice and Tangier disease patients with dysfunctional ABCA1 display a virtual absence of high-density lipoprotein (HDL), showing the essential role for ABCA1 in HDL metabolism. 3 Targeted inactivation of ABCA1 in bone marrow-derived cells in mice leads to increased atherosclerotic lesion formation, 4,5 whereas overexpression of ABCA1 inhibits the progression of atherosclerosis. 6 Macrophages lacking ABCA1, however, still have substantial ability to efflux cholesterol to HDL despite impaired efflux to lipid-poor apoAI, suggesting that macrophages have additional pathways via which cellular cholesterol can be exported. In addition to ABCA1, macrophages also express the ABC half-transporter ABCG1. In contrast to ABCA1, ABCG1 facilitates cellular cholesterol efflux from macrophages to mature HDL but not to lipid-free apolipopro- Methods and Results:

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Section: E28mentioning

confidence: 99%

Enhanced Foam Cell Formation, Atherosclerotic Lesion Development, and Inflammation by Combined Deletion of ABCA1 and SR-BI in Bone Marrow–Derived Cells in LDL Receptor Knockout Mice on Western-Type Diet

Zhao

Pennings

Hildebrand

et al. 2010

Circulation Research

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“…This notion was supported by the fact that C. pneumoniae is unlikely to cause systematic inflammation 28) . Experimental studies indicated that C. pneumoniae infection induced the production of cytokines from endothelial cells 29) , endothelial dysfunction 30) , and their lipopolysaccharide activated platelets 31) , leading to atherosclerosis and thrombogenesis.…”

Section: Discussionmentioning

confidence: 96%

Chlamydia pneumoniae Infection was Associated with Risk of Mortality from Coronary Heart Disease in Japanese Women but not Men: the JACC Study

Sakurai-Komada

Koike

Kaku

et al. 2010

JAT

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“…Macrophage regulation of growth of other host cells during embryogenesis, immune responses, or immunosurveillance might involve iron depletion [548] . Novel atherosclerotic markers indicating neutrophil activation represent Lf, an innate immune system protein with antiinflammatory and antioxidant properties [549,550] . Immunohistochemical staining of Lf was found in advanced human atherosclerotic carotid artery, as well as its co-localization with neutrophils and T and B lymphocytes in aortic plaques [551] .…”

Section: T Gondii Infectionmentioning

confidence: 99%

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

Prandota

2017

Journal of Cardiology and Therapy

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Multiple inflammatory markers in patients with significant coronary artery disease

Cited by 40 publications

References 23 publications

Enhanced Foam Cell Formation, Atherosclerotic Lesion Development, and Inflammation by Combined Deletion of ABCA1 and SR-BI in Bone Marrow–Derived Cells in LDL Receptor Knockout Mice on Western-Type Diet

Enhanced Foam Cell Formation, Atherosclerotic Lesion Development, and Inflammation by Combined Deletion of ABCA1 and SR-BI in Bone Marrow–Derived Cells in LDL Receptor Knockout Mice on Western-Type Diet

Chlamydia pneumoniae Infection was Associated with Risk of Mortality from Coronary Heart Disease in Japanese Women but not Men: the JACC Study

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

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