Highly oxidized low-density lipoprotein does not facilitate platelet aggregation

Miyazaki, Akira; Uehara, Takeshi; Usami, Yoko; Ishimine, Nau; Sugano, Mitsutoshi; Tozuka, Minoru

doi:10.1177/0300060520958960

Cited by 7 publications

(7 citation statements)

References 31 publications

(50 reference statements)

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“…The endothelial expression of ICAM-1 is increased in atherosclerotic cell cultures and in animal models of atherosclerosis. However, in vitro studies showed that ox-LDL may either activate or inhibit platelet function such as aggregation and β-thromboglobulin secretion [ 44 ], depending on the oxidized domain and the degree of oxidation [ 45 ]. These contradictions about platelet function inhibition and activation appear to stem from the heterogeneous nature of ox-LDL.…”

Section: Platelets As a Target Of Oxidized Ldlmentioning

confidence: 99%

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LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Rogula

Szarpak²,

Filipiak‬

2021

Life

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Atherosclerosis and its complications, including acute coronary syndromes, are the major cause of death worldwide. The two most important pathophysiological mechanisms underlying atherosclerosis include increased platelet activation and increased low-density lipoproteins (LDL) concentration. In contrast to LDL, oxidized (ox)-LDL have direct pro-thrombotic properties by functional interactions with platelets, leading to platelet activation and favoring thrombus formation. In this review, we summarize the currently available evidence on the interactions between LDL-cholesterol and platelets, which are based on (i) the presence of ox-LDL-binding sites on platelets, (ii) generation of ox-LDL by platelets and (iii) the role of activated platelets and ox-LDL in atherosclerosis. In addition, we elaborate on the clinical implications of these interactions, including development of the new therapeutic possibilities. The ability to understand and modulate mechanisms governing interactions between LDL-cholesterol and platelets may offer new treatment strategies for atherosclerosis prevention.

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Section: Platelets As a Target Of Oxidized Ldlmentioning

confidence: 99%

“…Both activated platelets and ox-LDL exert proinflammatory and procoagulant effects on several vascular cells (e.g., neutrophils, monocytes/macrophages, smooth muscle cells, endothelial cells, and platelets), thus supporting that atherosclerosis is a chronic inflammatory disease [ 44 , 49 ].…”

Section: Role Of Activates Platelets and Ox-ldl In Atherosclerosismentioning

confidence: 99%

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Rogula

Szarpak²,

Filipiak‬

2021

Life

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“…oxLDL plays a central role in the initiation and progression of atherosclerosis, as it mediates the promotion of several vascular cells (e.g., neutrophils, monocytes/macrophages, smooth muscle cells, endothelial cells, and platelets). Inflammatory and pro-regulatory effects ( 14 ). The primary mechanism of macrophage formation stems from disturbances in oxLDL uptake and lipid efflux.…”

Section: Discussionmentioning

confidence: 99%

Correlation Between Serum β2-GPI/oxLDL and the Risk of Cerebral Infarction in Patients with T2DM

Kuang

Liu

et al. 2022

Front. Surg.

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ObjectiveThis study aims to study the correlation between serum β2-glycoprotein I (β2-GPI)/oxidized low-density lipoprotein (oxLDL) and the risk of cerebral infarction in patients with type 2 diabetes (T2DM).MethodsFrom January 2019 to March 2021, 56 patients with T2DM combined with cerebral infarction were chosen as a diabetic cerebral infarction (DCI) group, and 60 patients with simple T2DM were chosen as a T2DM group. In addition, 60 healthy volunteers were recruited as a control group. The essential information of each group was collected, and the serum β2-GPI/oxLDL and inflammatory factor levels in each group were compared. The clinical factors that affect the risk of ischemic cerebral infarction in patients with T2DM were analyzed by a logistic model.ResultsCompared with the control group, the level of serum β2-GPI/oxLDL in the T2DM and DCI groups increased significantly, P < 0.001. Compared with the T2DM group, the serum β2-GPI/oxLDL level in the DCI group increased significantly, P < 0.05. The result of Pearson’s correlation analysis showed that serum β2-GPI/oxLDL was positively correlated with total cholesterol, triglycerides, fasting blood glucose, 2-h postprandial blood glucose, glycosylated hemoglobin, interleukin-6, and tumor necrosis factor (TNF)-α (all P’s < 0.05). Serum TNF-α and β2-GPI/oxLDL were independent risk variates for DCI (P < 0.05). Based on the receiver operating characteristic curve analysis, the values of the area under the curve for TNF-α, serum β2-GPI/oxLDL, and the combined diagnosis of DCI were 0.653 (0.552–0.753), 0.680 (0.583–0.777), 0.739 (0.647–0.831), respectively.ConclusionIn DCI patients, the levels of serum oxLDL/β2-GPI are significantly increased. Serum oxLDL/β2-GPI is an independent risk factor that affects the occurrence of DCI. In addition, the serum β2-GPI/oxLDL level implicates the lipid metabolism and inflammatory status of the internal environment of DCI patients to a certain extent.

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“…A possible reason is the complex action of lipids on platelets in the body. For example, naturally oxidized LDL can inhibit platelet aggregation 23 – 25 , which could partly explain the inconsistent results between in vivo and in vitro experiments.…”

Section: Discussionmentioning

confidence: 99%

Independent association of Lp(a) with platelet reactivity in subjects without statins or antiplatelet agents

Liu

Luo

et al. 2022

Sci Rep

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The physiological effect of Lp(a) on platelet activity is unclear. Previous studies explored the relationship between Lp(a) and platelet aggregation in patients taking statins and antiplatelet agents, but few was conducted in individuals without the bias of those drugs that either influence Lp(a) or platelet activity. The aim of this study was to assess the relationship between Lp(a) levels and platelet aggregation in subjects not taking statins or antiplatelet drugs. A hospital-based cross-sectional study was conducted to investigate the independent contribution of Lp(a) to platelet activity by controlling the effects of potential confounding factors including lipoprotein-associated phospholipase A2 [Lp-PLA2]. Blood samples were collected from 92 subjects without statins or antiplatelet agents from the Second Xiangya Hospital. The univariate correlation analysis showed a significant correlation between AA-induced average aggregation rate [AAR] and ApoB (r = 0.324, P = 0.002), ApoA1 (r = 0.252, P = 0.015), Lp(a) (r = 0.370, P < 0.001), Lp-PLA2 (r = 0.233, P = 0.025) and platelet counts [PLT] (r = 0.389, P < 0.001). Multivariate regression analysis suggested that Lp(a) contributed independently to AA-induced average aggregation rate (β = 0.023, P = 0.027) after controlling for the effects of ApoB, Lp-PLA2 and platelet counts. Lp(a) is positively associated with platelet aggregation independent of Lp-PLA2, which may partly account for the atherothrombotic effect of Lp(a).

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Highly oxidized low-density lipoprotein does not facilitate platelet aggregation

Cited by 7 publications

References 31 publications

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Correlation Between Serum β2-GPI/oxLDL and the Risk of Cerebral Infarction in Patients with T2DM

Independent association of Lp(a) with platelet reactivity in subjects without statins or antiplatelet agents

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