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Pasqui, Anna Laura; Puccetti, Luca; Bova, G; Renzo, M. Di; Bruni, Fulvio; Pastorelli, Marcello; Palazzuoli, Alberto; Auteri, Alberto

doi:10.1007/s102380200004

Cited by 20 publications

(8 citation statements)

References 20 publications

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“…Changes in sC5b-9 levels after treatment were inversely related to changes in HDL-C and total cholesterol levels. This is in line with previous studies demonstrating an inverse relationship between sC5b-9 and HDL-C [40]. This might be explained by the relationship between complement activation and inflammation, as both HDL-C and total cholesterol are known to increase with decreasing disease activity in IRDs [41].…”

Section: Discussionsupporting

confidence: 92%

Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study

et al. 2019

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Background The complement system is involved in pathogenesis of cardiovascular disease, and might play a role in accelerated atherogenesis in spondylarthropathies (SpA). Hence, we examined complement activation in SpA, and its relationship to antirheumatic treatment, inflammatory and cardiovascular markers. Methods From PSARA, a prospective observational study, we examined 51 SpA patients (31 psoriatic arthritis (PsA), and 20 ankylosing spondylitis (AS)), starting tumor necrosis factor (TNF) inhibitor alone (n = 25), combined with methotrexate (MTX) (n = 10), or MTX monotherapy (n = 16). Complement activation was determined by the soluble terminal complement complex (sC5b-9), inflammation by erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and endothelial function by finger plethysmography (Endopat) at baseline, after 6 weeks and 6 months of treatment. Results SpA patients had sC5b-9 levels at (PsA) or above (AS) the upper limit of the estimated reference range. Median sC5b-9 levels decreased significantly from baseline to 6 weeks, with no significant difference between the AS and PsA group. Notably, a significant reduction in sC5b-9 was observed after administration of TNF inhibitor ± MTX, whereas no significant changes were observed in patients treated with MTX alone. Between 6 weeks and 6 months, sC5b-9 remained stable across all subgroups. Reduction in sC5b-9 was independently related to decreased ESR and CRP, and to increased high density cholesterol and total cholesterol. Reduction in sC5b-9 from baseline to 6 weeks was associated with improved EF in age and gender adjusted analyses. Conclusion TNF-inhibition, but not MTX monotherapy, led to rapid and sustained reduction of complement activation in SpA. Thus, the observed decrease in cardiovascular morbidity in patients treated with TNF-inhibitors might be partly due to its beneficial effect on complement. Trial registration Clinical Trials ( NCT00902005 ), retrospectively registered on the 14 th of May 2009.

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Section: Discussionsupporting

confidence: 92%

Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study

et al. 2019

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“…Interestingly, the analysis of cultured endothelial cells has shown the blockage of membrane attack complex assembly by HDL [56,57]. On the contrary, in vivo studies have revealed a negative correlation between the HDL level and the concentration of the circulating terminal complex C5b-C9 in plasma [58]. These data are in contrast to the results of proteomic analysis.…”

Section: Immune Reactionsmentioning

confidence: 83%

High-Density Lipoproteins as Homeostatic Nanoparticles of Blood Plasma

Kudinov

Alekseeva

Torkhovskaya

et al. 2020

IJMS

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It is well known that blood lipoproteins (LPs) are multimolecular complexes of lipids and proteins that play a crucial role in lipid transport. High-density lipoproteins (HDL) are a class of blood plasma LPs that mediate reverse cholesterol transport (RCT)—cholesterol transport from the peripheral tissues to the liver. Due to this ability to promote cholesterol uptake from cell membranes, HDL possess antiatherogenic properties. This function was first observed at the end of the 1970s to the beginning of the 1980s, resulting in high interest in this class of LPs. It was shown that HDL are the prevalent class of LPs in several types of living organisms (from fishes to monkeys) with high resistance to atherosclerosis and cardiovascular disorders. Lately, understanding of the mechanisms of the antiatherogenic properties of HDL has significantly expanded. Besides the contribution to RCT, HDL have been shown to modulate inflammatory processes, blood clotting, and vasomotor responses. These particles also possess antioxidant properties and contribute to immune reactions and intercellular signaling. Herein, we review data on the structure and mechanisms of the pleiotropic biological functions of HDL from the point of view of their evolutionary role and complex dynamic nature.

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“…The complement system has been observed to directly participate in inflammation in atheromas [ 194 ], regulated by vitronectin and clusterin [ 195 ]. Likewise, in vitro assays have shown HDL can prevent organization of the membrane attack complex [ 196 , 197 ] and share a negative correlation with C5b-9 levels [ 198 ], promoting complement inhibition.…”

Section: Proteomics and Lipidomics: A Focus On Hdlmentioning

confidence: 99%

Dysfunctional High-Density Lipoprotein: An Innovative Target for Proteomics and Lipidomics

et al. 2015

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High-Density Lipoprotein-Cholesterol (HDL-C) is regarded as an important protective factor against cardiovascular disease, with abundant evidence of an inverse relationship between its serum levels and risk of cardiovascular disease, as well as various antiatherogenic, antioxidant, and anti-inflammatory properties. Nevertheless, observations of hereditary syndromes featuring scant HDL-C concentration in absence of premature atherosclerotic disease suggest HDL-C levels may not be the best predictor of cardiovascular disease. Indeed, the beneficial effects of HDL may not depend solely on their concentration, but also on their quality. Distinct subfractions of this lipoprotein appear to be constituted by specific protein-lipid conglomerates necessary for different physiologic and pathophysiologic functions. However, in a chronic inflammatory microenvironment, diverse components of the HDL proteome and lipid core suffer alterations, which propel a shift towards a dysfunctional state, where HDL-C becomes proatherogenic, prooxidant, and proinflammatory. This heterogeneity highlights the need for further specialized molecular studies in this aspect, in order to achieve a better understanding of this dysfunctional state; with an emphasis on the potential role for proteomics and lipidomics as valuable methods in the search of novel therapeutic approaches for cardiovascular disease.

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Cited by 20 publications

References 20 publications

Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study

Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study

High-Density Lipoproteins as Homeostatic Nanoparticles of Blood Plasma

Dysfunctional High-Density Lipoprotein: An Innovative Target for Proteomics and Lipidomics

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