Pharmacological modulation of vascular inflammation in atherothrombosis

Caterina, Raffaele De; Massaro, Marika; Scoditti, Egeria; Carluccio, Maria Annunziata

doi:10.1111/j.1749-6632.2010.05784.x

Cited by 21 publications

(18 citation statements)

References 77 publications

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“…Atherosclerosis is a complex mechanism that involves inflammatory processes, especially at the level of endothelial cells [37,38]. Several potential inflammatory biomarkers for the prediction of atherosclerosis have been proposed including CRP, IL-6, TNF-α, SELL, SELP, VCAM-1, ICAM-1 [39][40][41].…”

Section: Discussion/conclusionmentioning

confidence: 99%

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

et al. 2018

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Background: L-carnitine can be metabolized to trimethylamine N-oxide (TMAO), a molecule that promotes atherogenesis through its interaction with macrophages and lipid metabolism. Objective: The aim of the present study was to assess whether L-carnitine supplementation may promote changes in selected serum biomarkers of atherosclerosis. Methods: Before the start, in the mid-point and after completing the 24-weeks supplementation protocol, fasting blood samples were taken from the antecubital vein. Plasma free L-carnitine and TMAO were determined by the UPLC/MS/MS method. Serum proteins were determined by the enzyme immunoassay method using commercially available kits. Total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides have been determined using standard automatic analyzer. Results: L-carnitine supplementation elevated fasting plasma carnitine in the mid-point of our study and it remained increased until the end of supplementation period. Moreover, it induced tenfold increase in plasma TMAO concentration but did not affect serum C-reactive protein, interleukin-6, tumour necrosis factor-α, L-selectin, P-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 or lipid profile markers. Conclusion: We demonstrated that although oral L-carnitine supplementation significantly increased plasma TMAO concentration, no lipid profile changes or other markers of adverse cardiovascular events were detected in healthy aged women over the period of 24 weeks.

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Section: Discussion/conclusionmentioning

confidence: 99%

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

et al. 2018

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“…AP-1 plays an important role in endothelial inflammation by activating the expression of proinflammatory cytokines and other proteins relevant to vascular pathology, such as selectins and monocyte chemoattractant protein-1 45,46) . Several studies have demonstrated that the NF-ELAM-1 site activated by proinflammatory cytokines is recognized by AP-1 and not by the CRE-binding protein 43,47) .…”

Section: Discussionmentioning

confidence: 99%

Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation

Ito

Osaka

Edamatsu

et al. 2016

JAT

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Aim:The aryl hydrocarbon receptor (AhR), a ligand-inducible transcription factor mediating toxic effects of dioxins and uremic toxins, has recently emerged as a pathophysiological regulator of immune-inflammatory conditions. Indoxyl sulfate, a uremic toxin, is associated with cardiovascular disease in patients with chronic kidney disease and has been shown to be a ligand for AhR. The aim of this study was to investigate the potential role of AhR in indoxyl sulfate-induced leukocyte -endothelial interactions. Methods: Endothelial cell-specific AhR knockout (eAhR KO) mice were produced by crossing AhR floxed mice with Tie2 Cre mice. Indoxyl sulfate was administered for 2 weeks, followed by injection of TNF-. Leukocyte recruitment to the femoral artery was assessed by intravital microscopy. Vascular endothelial cells were transfected with siRNA specific to AhR (siAhR) and treated with indoxyl sulfate, followed by stimulation with TNF-. Results: Indoxyl sulfate dramatically enhanced TNF--induced leukocyte recruitment to the vascular wall in control animals but not in eAhR KO mice. In endothelial cells, siAhR significantly reduced indoxyl sulfate-enhanced leukocyte adhesion as well as E-selectin expression, whereas the activation of JNK and nuclear factor-B was not affected. A luciferase assay revealed that the region between 153 and 146 bps in the E-selectin promoter was responsible for indoxyl sulfate activity via AhR. Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Conclusion: AhR mediates indoxyl sulfate-enhanced leukocyte -endothelial interactions through AP-1 transcriptional activity, which may constitute a new mechanism of vascular inflammation in patients with renal disease.

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“…For example, benefits of 3 LC-PUFA from fish and fish oil have been observed at different stages of this disease process -including on plasma triglycerides [36][37] (arising from decreased endogenous synthesis and enhanced clearance of triglyceride-rich particles), on the size and the density of lipoprotein particles [38], thrombosis, inflammatory markers [39], blood pressure [29,33], vascular endothelium [30,33,40], proliferation of vascular smooth muscle and growth of atherosclerotic plaque [33,36,41], disorders of cardiac rhythm and sudden cardiac death [16,31,[42][43][44][45]. This review highlights some of the recent findings that demonstrate the effects of 3 LC-PUFA in influencing several key cardio-metabolic parameters, including hypertension, insulin resistance and diabetes in humans.…”

Section: Introductionmentioning

confidence: 99%

Role of ω3 Longchain Polyunsaturated Fatty Acids in Reducing Cardio- Metabolic Risk Factors

Abeywardena

Patten

2011

EMIDDT

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Cardiovascular disease is the leading cause of mortality in many economically developed nations, and its incidence is increasing at a rapid rate in emerging economies. Diet and lifestyle issues are closely associated with a myriad of cardiovascular disease risk factors including abnormal plasma lipids, hypertension, insulin resistance, diabetes and obesity, suggesting that diet-based approaches may be of benefit. Omega-3 longchain-polyunsaturated fatty acids (ω3 LC-PUFA) are increasingly being used in the prevention and management of several cardiovascular risk factors. Both the ω3 and ω6 PUFA families are considered essential, as the human body is itself unable to synthesize them. The conversion of the two precursor fatty acids - linoleic acid (18:2ω6) and α-linoleic acid (α18:3ω3) - of these two pathways to longer (≥C(20)) PUFA is inefficient. Although there is an abundance of ω6 PUFA in the food supply; in many populations the relative intake of ω3 LC-PUFA is low with health authorities advocating increased consumption. Fish oil, rich in eicosapentaenoic (EPA, 20:5ω3) and docosahexaenoic (DHA, 22:6ω3) acids, has been found to cause a modest reduction in blood pressure at a dose level of >3g/d both in untreated and treated hypertensives. Whilst a multitude of mechanisms may contribute to the blood pressure lowering action of ω3 LC-PUFA, improved vascular endothelial cell function appears to play a central role. Recent studies which evaluated the potential benefits of fish oil in type-2 diabetes have helped to alleviate concerns raised in some previous studies which used relatively large dose (5-8 g/d) and reported a worsening of glycemic control. Several meta-analyses have confirmed that the most consistent action of ω3 LC-PUFA in insulin resistance and type-2 diabetes is the reduction in triglycerides. In some studies, fish oil has been found to cause a small rise in LDL-cholesterol, but a change in the LDL particle size, from the smaller more atherogenic form to the larger, less damaging particle size, have also been noted. ω3 LC-PUFA are effective modulators of the inflammation that accompanies several cardio-metabolic abnormalities. Taking into consideration the pleiotropic nature of their actions, it can be concluded that dietary supplementation with ω3 LC-PUFA will lead to improvements in cardio-metabolic health parameters. These fatty acids pose only minor side effects and more importantly, do not interact adversely with the common drug therapies used in the management and treatment of hypertension, dyslipidemia, type-2 diabetes, and obesity/metabolic syndrome, but in some instances work synergistically, thereby providing additional cardiovascular benefits.

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Pharmacological modulation of vascular inflammation in atherothrombosis

Cited by 21 publications

References 77 publications

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation

Role of ω3 Longchain Polyunsaturated Fatty Acids in Reducing Cardio- Metabolic Risk Factors

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Pharmacological modulation of vascular inflammation in atherothrombosis

Cited by 21 publications

References 77 publications

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation

Role of &#x3C9;3 Longchain Polyunsaturated Fatty Acids in Reducing Cardio- Metabolic Risk Factors

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Role of ω3 Longchain Polyunsaturated Fatty Acids in Reducing Cardio- Metabolic Risk Factors