Lipoprotein-associated phospholipase A2 (Lp-PLA2) and tumor necrosis factor-alpha (TNF-α) and their relation to premature atherosclerosis in β-thalassemia children

Ragab, Seham M.; Safan, Manal A; Obeid, Osama M.; Sherief, Asmaa S.

doi:10.1179/1607845414y.0000000180

Cited by 27 publications

(13 citation statements)

References 64 publications

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“…Previous studies have shown that some cytokines(such as TNF-α, IL-1,8,12 and IFN-γ etc.) promote the occurrence of atherosclerosis 44 - 65 , while others(such as TNF-β, IL-4 and IL-10 etc.) inhibit the process of atherosclerosis 1 , 61 , 66 - 75 (see Table 1 ).…”

Section: Thymus Can Directly or Indirectly Modulate Inflammatory Procmentioning

confidence: 99%

The Pivotal Role of Thymus in Atherosclerosis Mediated by Immune and Inflammatory Response

et al. 2018

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Atherosclerosis is one kind of chronic inflammatory disease, in which multiple types of immune cells or factors are involved. Data from experimental and clinical studies on atherosclerosis have confirmed the key roles of immune cells and inflammation in such process. The thymus as a key organ in T lymphocyte ontogenesis has an important role in optimizing immune system function throughout the life, and dysfunction of thymus has been proved to be associated with severity of atherosclerosis. Based on previous research, we begin with the hypothesis that low density lipoprotein or cholesterol reduces the expression of the thymus transcription factor Foxn1 via low density lipoprotein receptors on the membrane surface and low density lipoprotein receptor related proteins on the cell surface, which cause the thymus function decline or degradation. The imbalance of T cell subgroups and the decrease of naive T cells due to thymus dysfunction cause the increase or decrease in the secretion of various inflammatory factors, which in turn aggravates or inhibits atherosclerosis progression and cardiovascular events. Hence, thymus may be the pivotal role in coronary heart disease mediated by atherosclerosis and cardiovascular events and it can imply a novel treatment strategy for the clinical management of patients with atherosclerosis in addition to different commercial drugs. Modulation of immune system by inducing thymus function may be a therapeutic approach for the prevention of atherosclerosis. Purpose of this review is to summarize and discuss the recent advances about the impact of thymus function on atherosclerosis by the data from animal or human studies and the potential mechanisms.

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Section: Thymus Can Directly or Indirectly Modulate Inflammatory Procmentioning

confidence: 99%

The Pivotal Role of Thymus in Atherosclerosis Mediated by Immune and Inflammatory Response

et al. 2018

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“…Among the pro-inflammatory cytokines, multiple studies have focused on TNF-α being an endogenous pyrogen, which can cause inflammation, apoptotic cell death, and mediate the release of variety cytokines like IL-6, IL-8 and IL-1β by stimulated macrophages [ 16 , 17 ]. Dysregulation, especially overproduction of TNF-α, has been found in a variety of human diseases including atherosclerosis [ 18 ], cancer [ 19 ], atherosclerosis [ 20 ] and inflammatory bowel disease [ 21 ]. However, it is still unclear, and many studies of depression are currently being connected to the TNF-α level.…”

Section: Introductionmentioning

confidence: 99%

Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Zhang

Baloch

2016

IJMS

167

100

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Major depressive disorder (MDD) is characterized by mood, vegetative, cognitive, and even psychotic symptoms and signs that can cause substantial impairments in quality of life and functioning. Up to now, the exact pathogenesis of MDD remains poorly understood. Recent research has begun to reveal that the pro-inflammatory cytokines, particularly, tumor necrosis factor-α (TNF-α), play an integral role in the pathophysiology of depressive disorders and the mechanism of antidepressant treatment. On the base of several observations: it is found that subsets of MDD patients have enhanced plasma levels TNF-α; antidepressant treatments had linked with the decline of TNF-α; central administration of TNF-α gives rise to sickness behavior which shares features with depression; and a blockade of it can ameliorate depressive symptomatology in animal models and clinical trials. In this review article, we focus on recent evidence linking TNF-α and MDD looking at data from animal and clinical studies, illustrating the pathophysiological role, susceptibility and its therapeutic application in depression. We conclude by discussing future directions for research, in particular the opportunities for the development of novel therapeutics that target TNF-α. This will be very important for designing preventative strategies and for the identification of new drug targets and preventative strategies.

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“…Lipoprotein-associated phospholipase A2 (Lp-PLA2) is excreted predominantly from atherosclerotic plaques by macrophages and neutrophils and subsequently circulates in the blood stream ( 10 ). It has been demonstrated that Lp-PLA2 is a potentially important pathogenic factor participating in the progression of atherosclerosis ( 11 ). In an animal model of hyperlipidemia and hyperglycemia, an Lp-PLA2 inhibitor reduced macrophage accumulation, and diminished the necrotic lipid-core volume and fibrous cap of coronary atherosclerotic plaques ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effect of rosuvastatin versus rosuvastatin/ezetimibe on markers of inflammation in patients with acute myocardial infarction

et al. 2017

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Statins lower low-density lipoprotein cholesterol (LDL-C) and high-sensitivity C-reactive protein (hsCRP), and the addition of ezetimibe to statins further reduces LDL-C and hsCRP. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a potentially important pathogenic factor participating in the progression of atherosclerosis. The aim of current study was to investigate how the addition of ezetimibe to rosuvastatin treatment affects reductions in LDL-C, hsCRP and Lp-PLA2 in patients with acute myocardial infarction (AMI). A total of 135 patients were enrolled in the study within 24 h of AMI, and were randomized to receive 10 mg rosuvastatin or 10 mg rosuvastatin plus 10 mg ezetimibe daily. HsCRP, Lp-PLA2, total cholesterol (TC), triglycerides (TG), LDL-C and high-density lipoprotein cholesterol (HDL-C) were determined at baseline and after 1, 3, 6 and 12 months of treatment. The addition of ezetimibe to rosuvastatin led to greater reduction of LDL-C compared with rosuvastatin monotherapy (from 3.00 to 1.19 mmol/l vs. 2.93 to 1.49 mmol/l, respectively; P<0.05), as well as reduced levels of hsCRP (from 5.15 to 0.68 mg/l vs. 4.33 to 1.49 mg/l, respectively; P<0.05) and Lp-PLA2 (from 333.13 to 79.07 mg/l vs. 327.95 to 123.62 mg/l, respectively; P<0.05). A positive association was identified between reductions of Lp-PLA2 and the changes of LDL-C (r=0.367; P=0.002). However, no significant correlation was observed between changes in Lp-PLA2 and hsCRP (r=0.264; P=0.512). The values of hsCRP and Lp-PLA2 appeared to increase during the first week after randomization, but dropped steeply to a lower level and remained stable thereafter. In conclusion, the addition of ezetimibe to rosuvastatin was demonstrated to further reduce LDL-C, hsCRP and Lp-PLA2 compared with rosuvastatin monotherapy in patients with AMI.

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Lipoprotein-associated phospholipase A2 (Lp-PLA2) and tumor necrosis factor-alpha (TNF-α) and their relation to premature atherosclerosis in β-thalassemia children

Cited by 27 publications

References 64 publications

The Pivotal Role of Thymus in Atherosclerosis Mediated by Immune and Inflammatory Response

The Pivotal Role of Thymus in Atherosclerosis Mediated by Immune and Inflammatory Response

Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Comparison of the effect of rosuvastatin versus rosuvastatin/ezetimibe on markers of inflammation in patients with acute myocardial infarction

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