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Nutrition and Nutritional Supplements in the Management of Dyslipidemia and Dyslipidemia-Induced Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The plant sterols are also anti-inflammatory and decrease the levels of proinflammatory cytokines such as interleukins (IL-6, IL1b) and TNF-α, as well as hsCRP, LpPLA 2, and fibrinogen; however, these effects vary among the various phytosterols [135]. Other potential mechanisms include modulation of signaling pathways, activation of cellular stress responses, cellular growth arrest, reduction of Apo-B48 secretion from intestinal and hepatic cells, reduction of cholesterol synthesis with suppression of HMG-CoA reductase and cytochrome P 450 (CYP7A1), interference with SREBP, and promotion of RCT via ABCA1 and ABCG1 [135]. The biological activity of phytosterols is both cell-type and sterol-specific [133].
Innate Immune System in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Benjamin J. Kopecky, Kory J. Lavine
Macrophages in atherosclerotic plaques are predominantly derived from circulating monocytes [90]. In murine models, hypercholesterolemia promotes selective expansion of classical monocytes through CSF1- and IL-3-dependent extramedullary hematopoiesis [90]. In humans, classical CD14high CD16low monocytes are increased in hyper-cholesterolemia [91]. Subendothelial retention of low-density lipoprotein (LDL) and local production of CCL2, CCL20, and sphingosine-1-phosphate recruit monocytes to the site of arterial inflammation [92, 93]. Suppression of monocyte recruitment led to plaque regression [94]. Myeloid-specific depletion of ATP-binding cassette transporters (ABCA1 and ABCG1), which are important in the efflux of LDL to high-density lipoprotein (HDL), led to increased atherosclerosis and monocytosis [95].
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Genetically engineered disruption of cholesterol metabolism defines the two major models of atherosclerosis; apolipoprotein E-deficient (ApoE+) and LDL receptor (LDLR)-deficient mice develop two ApoE and other mice deficient in lipid-efflux proteins, such as the adenosine triphosphate (ATP)-binding cassette transporter 1 (ABCA1) and ATP-binding cassette transporter 1 (ABCAA1) and ATP-binding cassette subfamily G member 1 (ABCG1), have forged a mechanistic link between leukocyte and lipid biology. Trapped cholesterol in hematopoietic stem and progenitor cells (HSPCs) that lack the crucial cholesterol efflux machinery leads to the expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-3 common beta chain receptor on the plasma membrane contributes to excessive proliferation.247,248 In other words, cholesterol efflux suppress proliferation. Concurrently, lipid-rich splenic phagocytes release IL-23, which induces a cascade that eventually liberates HSPCs from their medullary niches.249 When HSPCs seed extramedullary sites, they encounter GM-CSF and IL-3.250 The net effect is HSPC proliferation, extramedullary hematopoiesis, leukocytosis, and accelerated atherosclerosis.
Impact of DNA methylation on ADME gene expression, drug disposition, and efficacy
Published in Drug Metabolism Reviews, 2022
Xu Hao, Yuanyuan Li, Jialu Bian, Ying Zhang, Shiyu He, Feng Yu, Yufei Feng, Lin Huang
Higher ABCA1 cg14019050 methylation was correlated with lower ABCA1 gene expression in the ENCODE consortium has been reported by Ma et al. (Ma et al. 2016). The negative correlation between ABCB1 promoter methylation and gene expression has been proved in some cancer cell lines and MDR resistance models. The corresponding CpG sites are located downstream of TSS (+524, +526, +554, +556, +580, +583, +587) (Spitzwieser et al. 2016). Liu et al. found that ABCG1 gene expression was negatively correlated with ABCG1 methylation site cg06500161 in all nondiabetic participants in the Framingham Heart Study Offspring (Liu et al. 2020). Methylation bands were present but ABCG2 gene expression was not detected in SUN-C4, Colo201, LS174T, and SW480. And the CpG island region (−136 to −417) contains 21 CpG dinucleotide sites and is part of the promoter for the ABCG2 gene (Moon et al. 2016). The SLC5A8 transcriptional repression was associated with abnormal methylation of a 379-bp (+123 to +501) region, which contains 45 CpG sites (Hernandez-Juarez et al. 2019). Chen et al. confirmed that the significant down-regulation of OCT1 mRNA expression in hepatocellular carcinoma was explained by methylation of specific CpG sites, that is, cg13466809 and cg27292431 in the 5′-UTR and exon 1 of the SLC22A1 gene (Chen, Neul, et al. 2020).
An inflammatory triangle in Sarcoidosis: PPAR-γ, immune microenvironment, and inflammation
Published in Expert Opinion on Biological Therapy, 2021
Parnia Jabbari, Mona Sadeghalvad, Nima Rezaei
As mentioned earlier, healthy people take advantage of the high-level of PPAR-γ in alveolar macrophages [48,49]. PPAR-γ keeps pulmonary lipid homeostasis stable through inducing the expression of alveolar macrophage ATP-binding cassette lipid transporter-G1 (ABCG1) [63]. ABCG1 is essential to keep pulmonary lipid homeostasis [64]. Lipids are uptake to the alveolar macrophages by scavenger receptors like CD36 [65]. ABCG1 has an important role in the effluxion of catabolized lipids to the extracellular matrix, the process which is enhanced by another complementary transporter named ABCA1 [66]. Lack of ABCG1 or ABCA1 triggers pulmonary lipid accumulation, pro-inflammatory macrophage activation, and increased-inflammatory mediators, which leads to lung inflammation and fibrosis [67,68]. So, the transporter ABCG1 or ABCA1 could be considered as other PPAR-γ targets for keeping pulmonary homeostasis.
Biologics and atherosclerotic cardiovascular risk in rheumatoid arthritis: a review of evidence and mechanistic insights
Published in Expert Review of Clinical Immunology, 2021
George A Karpouzas, Viet L Bui, Nicoletta Ronda, Ivana Hollan, Sarah R Ormseth
Qualitative and functional differences in lipoproteins in RA may further complicate the impact of lipid metabolism on atherosclerosis. An isolated quantitative evaluation of serum lipid levels may, therefore, be insufficient to characterize CVD risk. LDL alteration includes increased oxidation rate of both LDL and Lp(α) [53]. The lipidome of small, dense HDL may be altered in RA and higher inflammation may associate with functional deficiency of small, dense HDL [54]. Moreover, HDL dysfunction in RA includes the reduction of both their anti-inflammatory/anti-oxidant properties [55] and their cholesterol efflux capacity (CEC) [56,57]. HDL normally inhibits LDL oxidation through the release of antioxidant enzymes. Additionally, it inhibits adhesion molecule expression in endothelial cells [58]. Inflammation-associated oxidative stress is linked to lower levels of ApoAI and paroxonase 1, higher serum alpha amyloid, and oxidized fatty acids in the HLD particle, leading to a proinflammatory behavior of HDL [59–61]. HDL promotes cell cholesterol efflux through the transporters ATP binding cassette A1 (ABCA1) and G1 (ABCG1), and through the Scavenger receptor type B class I (SR-BI). ABCG1 CEC, particularly sensitive to inflammation, was impaired in RA and inversely related to the disease activity score (DAS28) in a recent study [56].