Oxidised Low Density Lipoprotein (LDL) Modification with Statin Therapy is Associated with Reduction in Carotid Stenosis

Skopelitis, Elias; Levisianou, D.; Lydataki, Helen; SofoklisKougialis,

doi:10.5772/57188

Cited by 3 publications

(7 citation statements)

References 68 publications

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“…Recent findings point to hypercholesterolemia as a primary cause of endothelial dysfunction by altering endothelial permeability, enabling low-density lipoproteincholesterol (LDL-c) to migrate into the arterial wall LDL-c may migrate into the artery wall because of hypercholesterolemia's capacity to change the arterial permeability, causing endothelial dysfunction [11]. Absorption of LDL by monocyte-derived macrophages via scavenger receptor (SR) that are not limited by cell cholesterol levels and can bind both ox-LDL and native lipoproteins is facilitated by the macrophage receptor recognition shift toward LDL due to oxidative modification [12,13]. Foam cells, which are characteristic of fatty streak and collect lipids in their cytoplasm because of SR's activity, are seen in macrophages [14][15][16].…”

Section: The Origin Of Atherosclerosis and The Formation Of Fatty Str...mentioning

confidence: 99%

Pathogenesis of Atherosclerosis: Review

Ayoub

2022

JPRI

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In atherosclerosis, apolipoprotein B-lipoproteins in blood artery matrix attract monocytes, which become macrophages and dendritic cells. Macrophages generated from recruited monocytes cause a maladaptive, non-resolving inflammatory response that increases subendothelial layer. Some lesions cause myocardial infarction, stroke, and sudden cardiac death. Modern atherosclerosis research focuses on the molecular biology of atherogenesis, although the disease's complex pathophysiology is still unknown. The goal of this research is to examine the mechanisms of atherosclerosis development, such as endothelial dysfunction, fatty streak formation, fibrous plaque formation, and plaque rupture (Fig. 1.). This article takes a thorough look at the pathophysiology of atherosclerosis, addressing the pathological and biochemical mechanisms of atherosclerotic plaque development and growth. Atherosclerosis pathogenesis and disease development are the primary topics of discussion in this review, which focuses on the disease's particular targets.

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Section: The Origin Of Atherosclerosis and The Formation Of Fatty Str...mentioning

confidence: 99%

Pathogenesis of Atherosclerosis: Review

Ayoub

2022

JPRI

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“…Main pathogenesis process involved in atherosclerosis. [28,29]. ROS are defined as oxygen molecule (O 2 ) that accepts a single electron where it transformed into highly reactive radicals that damage cellular lipids, proteins and DNA [30].…”

Section: Trapping and Oxidation Of Low-density Lipoprotein Cholesteromentioning

confidence: 99%

“…The macrophage receptor recognition shift toward LDL due to its oxidative modification causes uptake of LDL by monocyte-derived macrophages via SR that are not regulated by cholesterol content of the cell and these receptors can bind a variety of ligands such as Ox-LDL and native lipoproteins [29,32]. It is due to the function of SR there will be massive accumulation of lipids within the cytoplasm of macrophages giving picture of foamy appearance to these cells; hence, these cells have been named as foam cells and regarded as the hallmark of fatty streak [25,31,33].…”

Section: The Pathological Hallmark Of Fatty Streak Developmentmentioning

confidence: 99%

“…Oxidized LDL induces the endothelial cells to produce inflammatory mediators and to express adhesion molecules, this, in turn, will drive inflammatory process and immune cell infiltration at the lesion sites [22]. Oxidized LDL is implicated in the following pathogenic effects: upregulation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), selectins and chemoattractants such as lipids, platelets-activating factor, and chemokines such as interleukin-8 and monocyte chemoattractant protein-1 (MCP-1) [29,34]. Circulating monocytes become adherent to the activated endothelial cells, this adhesion process will be followed by migration of monocytes by process of diapedesis through intercellular junctions to the subendothelial space [32].…”

Section: The Pathological Hallmark Of Fatty Streak Developmentmentioning

confidence: 99%

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Basic pathogenic mechanisms of atherosclerosis

Alfarisi

Mohamed

Ibrahim

2020

Egyptian Journal of Basic and Applied Sciences

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Atherosclerosis is a chronic inflammatory disease of the inner wall of largeand medium-sized arteries. It is a disease of multiple causes which regarded as the primary underlying cause of heart diseases and cerebrovascular accidents. Pathologically, atherosclerosis is a chronic arterial inflammation secondary to prolonged exposure to oxidative stressors and involves multiple cell types and cellular mediators. Oxidized lipids derived from low-density lipoprotein contribute to multiple stages of atherosclerotic plaque development and progression through production of inflammatory cytokines. Diet and dietary habits are the major driving forces for development and modification of atherosclerotic diseases. Genetics and epigenetics have a significant influence on development and progression of atherosclerosis. Future therapeutic options may target the pathogenic mediators of atherosclerosis at multiple molecular levels.

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“…The intensity of the color formed is proportional to the triglycerides concentration in the sample . The lipoproteins of VLDL, and LDL contained in the serum sample were precipitates by the addition by the addition of (4%) phosphotungstic acid solution, which contain (10%) magnesium chloride (PH 6.2) .The supernatant obtained after centrifugation contains the HDL, from which the cholesterol can be determined by complementary kit used in determination of total serum cholesterol as described in reference (7) .LDL-cholesterol and VLDLwere estimated indirectly by using Fried Ewald formula (8) :-…”

Section: Laboratory Testsmentioning

confidence: 99%

Assessment of Serum Visfatin Levels in Patients with Chronic Obstructive Pulmonary Diseases in Babylon-Iraq

Salman¹,

Al-joda²,

Alshok³

2020

IJFMT

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The presented study aims to evaluate of the levels of serum Visfatin, in patients with chronic obstructive Pulmonary diseases in Babylon-Iraq , to find the correlation of Visfatin, with lipid profile in these patients and compared with apparently healthy as case -control study. The study included (50) patients as patients group diagnosed with COPD (G1) and ( 50)as apparently control group(G2) .The age of all studied groups ranged between (40-65)years and BMI with (18.8-24.4) Kg/m 2 .Serum was used in determination of FBS, lipid profile( Ch,TG,HDL-c,LDL-c and VLDL-c) , insulin , CRP and Visfatin , Whole blood was used for determination of HbA1C . The results revealed significant elevation in FBG and HbA1c levels were seen in patients groups when comparing to healthy control .The results indicates a significant elevation in TC, TG ,LDL-c and VLDL-c in G1 comparing to G2. Also , HDL-c significant decreased in G1 comparing to G 2 , Also ,the results showed significant increased in CRP levels in G1 , when comparing to G2, A non significant visfatin and insulin level in G1 when compared with G2(p value = 0.486) , . A non significant correlation was found in G1 between visfatin ,TC,TG, HDL-c and VLDL-c.The conclusion from this study indicate that G1 which HDL-c is low in this group has the highest value for FBS , HbA1c , TC ,TG,LDL and VLDL .Also, the study found non correlation between lipid profile parameters in G1

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Oxidised Low Density Lipoprotein (LDL) Modification with Statin Therapy is Associated with Reduction in Carotid Stenosis

Cited by 3 publications

References 68 publications

Pathogenesis of Atherosclerosis: Review

Pathogenesis of Atherosclerosis: Review

Basic pathogenic mechanisms of atherosclerosis

Assessment of Serum Visfatin Levels in Patients with Chronic Obstructive Pulmonary Diseases in Babylon-Iraq

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