Malondialdehyde-modified low-density lipoproteins as biomarker for atherosclerosis

Viigimaa, Margus; Abina, Jelena; Zemtsovskaya, Galina; Tikhaze, A. K.; Konovalova, G. G.; Kumskova, E. M.; Ланкин, В. З.

doi:10.3109/08037051.2010.484158

Cited by 42 publications

(21 citation statements)

References 11 publications

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“…114 Malondialdehyde-modified oxidized low-density lipoproteins (oxLDL) are implicated in CVD in general, 115 and especially in SLE-associated CVD. 114 HDL, but not oxHDL, protects against the atherogenic effects of oxLDL.…”

Section: Oxidative Stress and T-cell Dysfunctionmentioning

confidence: 99%

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Oxidative stress in the pathology and treatment of systemic lupus erythematosus

2013

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Oxidative stress is increased in systemic lupus erythematosus (SLE), and it contributes to immune system dysregulation, abnormal activation and processing of cell-death signals, autoantibody production and fatal comorbidities. Mitochondrial dysfunction in T cells promotes the release of highly diffusible inflammatory lipid hydroperoxides, which spread oxidative stress to other intracellular organelles and through the bloodstream. Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE. In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine-protein kinase mTOR undergoes redox-dependent activation. In turn, reversal of glutathione depletion by application of its amino acid precursor, N-acetylcysteine, improves disease activity in lupus-prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research. Blocking mTOR activation in T cells could conceivably provide a well-tolerated and inexpensive alternative approach to B-cell blockade and traditional immunosuppressive treatments. Nevertheless, compartmentalized oxidative stress in self-reactive T cells, B cells and phagocytic cells might serve to limit autoimmunity and its inhibition could be detrimental. Antioxidant therapy might also be useful in ameliorating damage caused by other treatments. This Review thus seeks to critically evaluate the complexity of oxidative stress and its relevance to the pathogenesis and treatment of SLE.

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Section: Oxidative Stress and T-cell Dysfunctionmentioning

confidence: 99%

“…119 As mentioned in the section on comorbidities, oxHDL is associated with atherosclerosis in SLE, 100 and oxLDL is a biomarker of CVD. 115 …”

Section: Clinical Approaches and Implicationsmentioning

confidence: 99%

Oxidative stress in the pathology and treatment of systemic lupus erythematosus

2013

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“…Some cross-sectional studies have shown a significant correlation between serum levels of MDA-LDL and LDL-C 34, 35 and coronary endothelial function. 36 In the present study, we also found that the MDA-LDL/ LDL-C ratio increased in the ezetimibe addition group despite the lack of significant reductions in serum LDL-C and MDA-LDL, and the ratio did not change with increasing the dose of atorvastatin.…”

Section: -31mentioning

confidence: 99%

Differences in Action of Atorvastatin and Ezetimibe in Lowering Low-Density Lipoprotein Cholesterol and Effect on Endothelial Function

Matsue

Matsumura

Hashimoto

et al. 2013

Circ J

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Background:The aim of this study was to compare the effect on endothelial function of increasing statin dose to add-on ezetimibe in patients with coronary artery disease (CAD) already treated with statin. Methods and Results:Two-hundred and forty-three patients with CAD and low-density lipoprotein cholesterol (LDL-C) ≥70 mg/dl even after treatment with atorvastatin (10 mg) were prospectively randomized to the ezetimibe addition (10 mg) group (A10E10; n=117) or to the double atorvastatin dose (to 20 mg; A20; n=133) group for 12 weeks. Primary endpoint was change in endothelial function measured by logarithmic-scale reactive hyperemia index (L_RHI). After treatment, high-sensitivity C-reactive protein (hs-CRP) and all lipids except triglyceride and highdensity lipoprotein cholesterol were significantly reduced in both groups. The mean percent changes in LDL-C for the A10E10 and A20 groups were -25.8% and -9.1%, respectively (P<0.001). L_RHI increased from 0.47 to 0.62 in the A20 group (P<0.001), but not in the A10E10 group (from 0.45 to 0.48, P=0.399). Absolute change in L_RHI was significantly higher in the A20 than A10E10 group (0.02±0.29 vs. 0.16±0.27, P<0.001).Conclusions: Statin and ezetimibe have different effects on endothelial function independent from LDL-C-lowering effects. (Circ J 2013; 77: 1791 -1798

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“…The polyunsaturated fatty acids in cholesteryl esters, phospholipids and triglycerides are also subjected to free radical-initiated oxidation to yield a broad array of smaller fragments (Matsuura et al, 2008). This results in a variety of reactive aldehyde products, including (E)-4-hydroxynon-2-enal (HNE) and malondialdehyde (MDA), which form covalent adducts with amino acid residues of LDL, generating HNE-LDL and MDA-LDL, respectively (Annangudi et al, 2008;Viigimaa et al, 2010). Glycated LDL is formed by the nonenzymatic covalent binding of reactive aldehydes (from glucose or related species) to a reactive amine (e.g., lysine and arginine side chains) on apoB-100 (Brown et al, 2007).…”

Section: Ldl and Its Modified Formsmentioning

confidence: 99%