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Статті в журналах з теми "Proteomics, fatty acids, cardiovascular disease"

Автор: Grafiati
Опубліковано: 11 березня 2023

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1

Zhang, Yang, Ao Zhang, Laidi Wang, Ting Yang, Bingqiang Dong, Zhixiu Wang, Yulin Bi, Guohong Chen, and Guobin Chang. "Metabolomics and Proteomics Characterizing Hepatic Reactions to Dietary Linseed Oil in Duck." International Journal of Molecular Sciences 23, no. 24 (December 10, 2022): 15690. http://dx.doi.org/10.3390/ijms232415690.

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Анотація:
The imbalance in polyunsaturated fatty acid (PUFA) composition in human food is ubiquitous and closely related to obesity and cardiovascular diseases. The development of n-3 PUFA-enriched poultry products is of great significance for optimizing fatty acid composition. This study aimed to improve our understanding of the effects of dietary linseed oil on hepatic metabolism using untargeted metabolomics and 4D label-free proteome analysis. A total of 91 metabolites and 63 proteins showed differences in abundance in duck livers between the high linseed oil and control groups. Pathway analysis revealed that the biosynthesis of unsaturated fatty acids, linoleic acid, glycerophospholipid, and pyrimidine metabolisms were significantly enriched in ducks fed with linseed oil. Meanwhile, dietary linseed oil changed liver fatty acid composition, which was reflected in the increase in the abundance of downstream metabolites, such as α-linolenic acid (ALA; 18:3n-3) as a substrate, including n-3 PUFA and its related glycerophospholipids, and a decrease in downstream n-6 PUFA synthesis using linoleic acid (LA; 18:2n-6) as a substrate. Moreover, the anabolism of PUFA in duck livers showed substrate-dependent effects, and the expression of related proteins in the process of fatty acid anabolism, such as FADS2, LPIN2, and PLA2G4A, were significantly regulated by linseed oil. Collectively, our work highlights the ALA substrate dependence during n-3 PUFA synthesis in duck livers. The present study expands our knowledge of the process products of PUFA metabolism and provides some potential biomarkers for liver health.
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2

Wu, Ping-Hsun, Yi-Wen Chiu, Hsin-Bai Zou, Cheng-Chih Hsu, Su-Chu Lee, Yi-Ting Lin, Yi-Chun Tsai, Mei-Chuan Kuo, and Shang-Jyh Hwang. "Exploring the Benefit of 2-Methylbutyric Acid in Patients Undergoing Hemodialysis Using a Cardiovascular Proteomics Approach." Nutrients 11, no. 12 (December 12, 2019): 3033. http://dx.doi.org/10.3390/nu11123033.

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Short-chain fatty acids (SCFAs) can reduce pro-inflammatory parameters and oxidative stress, providing potential cardiovascular (CV) benefits. Although some evidence links SCFAs with host metabolic health via several biological mechanisms, the role of SCFA on CV disease in patients with kidney disease remains unclear. Herein, we investigate the association between a SCFA, 2-methylbutyric acid, and target CV proteomics to explore the potential pathophysiology of SCFA-related CV benefit in patients with kidney disease. Circulating 2-methylbutyric acid was quantified by high-performance liquid chromatography and 181 CV proteins by a proximity extension assay in 163 patients undergoing hemodialysis (HD). The associations between 2-methylbutyric acid and CV proteins were evaluated using linear regression analysis with age and gender, and multiple testing adjustment. The selected CV protein in the discovery phase was further confirmed in multivariable-adjusted models and evaluated by continuous scale association. The mean value of circulating 2-methylbutyric acid was 0.22 ± 0.02 µM, which was negatively associated with bone morphogenetic protein 6 (BMP-6) according to the false discovery rate (FDR) multiple testing adjustment method. The 2-methylbutyric acid level remained negatively associated with BMP-6 (β coefficient −1.00, 95% confidence interval −1.45 to −0.55, p < 0.001) after controlling for other CV risk factors in multivariable models. The cubic spline curve demonstrated a linear relationship. In conclusion, circulating 2-methylbutyric acid level was negatively associated with BMP-6, suggesting that this pathway maybe involved in vascular health in patients undergoing HD. However, further in vitro work is still needed to validate the translation of the mechanistic pathways.
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3

Olin, Jeffrey W., Antonio F. Di Narzo, Valentina d’Escamard, Daniella Kadian-Dodov, Haoxiang Cheng, Adrien Georges, Annette King, et al. "A plasma proteogenomic signature for fibromuscular dysplasia." Cardiovascular Research 116, no. 1 (August 19, 2019): 63–77. http://dx.doi.org/10.1093/cvr/cvz219.

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Abstract Aims Fibromuscular dysplasia (FMD) is a poorly understood disease that predominantly affects women during middle-life, with features that include stenosis, aneurysm, and dissection of medium-large arteries. Recently, plasma proteomics has emerged as an important means to understand cardiovascular diseases. Our objectives were: (i) to characterize plasma proteins and determine if any exhibit differential abundance in FMD subjects vs. matched healthy controls and (ii) to leverage these protein data to conduct systems analyses to provide biologic insights on FMD, and explore if this could be developed into a blood-based FMD test. Methods and results Females with ‘multifocal’ FMD and matched healthy controls underwent clinical phenotyping, dermal biopsy, and blood draw. Using dual-capture proximity extension assay and nuclear magnetic resonance-spectroscopy, we evaluated plasma levels of 981 proteins and 31 lipid sub-classes, respectively. In a discovery cohort (Ncases = 90, Ncontrols = 100), we identified 105 proteins and 16 lipid sub-classes (predominantly triglycerides and fatty acids) with differential plasma abundance in FMD cases vs. controls. In an independent cohort (Ncases = 23, Ncontrols = 28), we successfully validated 37 plasma proteins and 10 lipid sub-classes with differential abundance. Among these, 5/37 proteins exhibited genetic control and Bayesian analyses identified 3 of these as potential upstream drivers of FMD. In a 3rd cohort (Ncases = 506, Ncontrols = 876) the genetic locus of one of these upstream disease drivers, CD2-associated protein (CD2AP), was independently validated as being associated with risk of having FMD (odds ratios = 1.36; P = 0.0003). Immune-fluorescence staining identified that CD2AP is expressed by the endothelium of medium-large arteries. Finally, machine learning trained on the discovery cohort was used to develop a test for FMD. When independently applied to the validation cohort, the test showed a c-statistic of 0.73 and sensitivity of 78.3%. Conclusion FMD exhibits a plasma proteogenomic and lipid signature that includes potential causative disease drivers, and which holds promise for developing a blood-based test for this disease.
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4

Méndez, Lucía, Silvia Muñoz, Bernat Miralles-Pérez, Maria Rosa Nogués, Sara Ramos-Romero, Josep Lluis Torres, and Isabel Medina. "Modulation of the Liver Protein Carbonylome by the Combined Effect of Marine Omega-3 PUFAs and Grape Polyphenols Supplementation in Rats Fed an Obesogenic High Fat and High Sucrose Diet." Marine Drugs 18, no. 1 (December 30, 2019): 34. http://dx.doi.org/10.3390/md18010034.

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Diet-induced obesity has been linked to metabolic disorders such as cardiovascular diseases and type 2 diabetes. A factor linking diet to metabolic disorders is oxidative stress, which can damage biomolecules, especially proteins. The present study was designed to investigate the effect of marine omega-3 polyunsaturated fatty acids (PUFAs) (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) and their combination with grape seed polyphenols (GSE) on carbonyl-modified proteins from plasma and liver in Wistar Kyoto rats fed an obesogenic diet, namely high-fat and high-sucrose (HFHS) diet. A proteomics approach consisting of fluorescein 5-thiosemicarbazide (FTSC) labelling of protein carbonyls, visualization of FTSC-labelled protein on 1-DE or 2-DE gels, and protein identification by MS/MS was used for the protein oxidation assessment. Results showed the efficiency of the combination of both bioactive compounds in decreasing the total protein carbonylation induced by HFHS diet in both plasma and liver. The analysis of carbonylated protein targets, also referred to as the ‘carbonylome’, revealed an individual response of liver proteins to supplements and a modulatory effect on specific metabolic pathways and processes due to, at least in part, the control exerted by the supplements on the liver protein carbonylome. This investigation highlights the additive effect of dietary fish oils and grape seed polyphenols in modulating in vivo oxidative damage of proteins induced by the consumption of HFHS diets.
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5

Pratt, Charlotte, and Sam Feudo. "A Portfolio Analysis of Nutritional Biomarkers in NIH- and NHLBI-funded Research, 2008–2020." Current Developments in Nutrition 6, Supplement_1 (June 2022): 390. http://dx.doi.org/10.1093/cdn/nzac054.045.

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Abstract Objectives Nutrition biomarkers are important in elucidating disease risks and severity, as surrogate markers of nutritional status, and provide objective measures of dietary intake. This study analyzed grants that investigated nutritional biomarkers and were funded between 2008 and 2020 by the National Heart, Lung, and Blood Institute (NHLBI) and across the National Institutes of Health (NIH). Methods Data were extracted using the NIH iSearch portfolio analysis platform to curate grant applications to the NIH and NHLBI. Keywords included nutrition or diet, followed by omics, metabolomics, lipidomics, proteomics, transcriptomics, genomics, and epigenomics. Funded and unfunded nutri-omics grants were separated and examined for keywords for total expenditures, Research, Condition, and Disease Categorization (RCDC) categories, administering Institute, fiscal year, Early-Stage Investigator eligibility, and organization. Citation and publication data stemming from each awarded grant were collated using iCite. Results The total number of NIH- and NHLBI-funded grants in nutri-omics biomarkers was 1,143 and 95, respectively from 2008–2020. Total dollar amount of NIH-funded grants in nutri-omics biomarkers increased from $15M in 2008 to $59.5M in 2019 and declined to $47M in 2020. NHLBI funded grants increased substantially during the same years from $1.8M in 2008 to $7.5M in 2020. During the 12-year period, the proportion of ESI grants among funded grants increased by about 10-fold across NIH and 2-fold for NHLBI. There was an increase in the number of NHLBI research publications (500%) and relative citation ratios (RCR) (150%). Funded grants were concentrated along the East and West coasts of the United States. Major foam tree topics from NHLBI-administered nutri-omics grants included cardiovascular disease, dietary patterns, obesity, human genome, risk factors, microbiome, TMAO (trimethyl amine oxide), and fatty acids. Conclusions The analysis indicated increased funding in nutri-omics biomarkers. However, major gaps remain in topics categorized as nutrition biomarkers in NHLBI- and NIH-funded grants. More research is needed to characterize and examine novel biomarkers in NIH-funded grants. Funding Sources Not applicable.
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6

Lecerf, Jean-Michel. "Fatty acids and cardiovascular disease." Nutrition Reviews 67, no. 5 (May 2009): 273–83. http://dx.doi.org/10.1111/j.1753-4887.2009.00194.x.

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7

Mozaffarian, Dariush, Martijn B. Katan, Alberto Ascherio, Meir J. Stampfer, and Walter C. Willett. "Trans Fatty Acids and Cardiovascular Disease." New England Journal of Medicine 354, no. 15 (April 13, 2006): 1601–13. http://dx.doi.org/10.1056/nejmra054035.

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8

Richard, Doriane, Pedro Bausero, Charlotte Schneider, and Francesco Visioli. "Polyunsaturated fatty acids and cardiovascular disease." Cellular and Molecular Life Sciences 66, no. 20 (July 10, 2009): 3277–88. http://dx.doi.org/10.1007/s00018-009-0085-4.

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9

Salter, A. M. "Dietary fatty acids and cardiovascular disease." Animal 7 (2013): 163–71. http://dx.doi.org/10.1017/s1751731111002023.

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10

Mozaffarian, Dariush, Martijn B. Katan, Alberto Ascherio, Meir J. Stampfer, and Walter C. Willett. "Trans Fatty Acids and Cardiovascular Disease." Obstetrical & Gynecological Survey 61, no. 8 (August 2006): 525–26. http://dx.doi.org/10.1097/01.ogx.0000228706.09374.e7.

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11

Calzolari, Ivan, Stefano Fumagalli, Niccolo Marchionni, and Mauro Di Bari. "Polyunsaturated Fatty Acids and Cardiovascular Disease." Current Pharmaceutical Design 15, no. 36 (December 1, 2009): 4094–102. http://dx.doi.org/10.2174/138161209789909755.

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12

Elisaf, M. S., A. M. Liontos, T. D. Filippatos, and M. Georgoula. "Trans Fatty Acids and Cardiovascular Disease Risk." Journal of Nutritional Therapeutics 3, no. 2 (June 16, 2014): 47–49. http://dx.doi.org/10.6000/1929-5634.2014.03.02.2.

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13

Grundt, H., and D. W. T. Nilsen. "n-3 fatty acids and cardiovascular disease." Haematologica 93, no. 6 (June 1, 2008): 807–12. http://dx.doi.org/10.3324/haematol.13191.

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14

De Caterina, Raffaele. "n–3 Fatty Acids in Cardiovascular Disease." New England Journal of Medicine 364, no. 25 (June 23, 2011): 2439–50. http://dx.doi.org/10.1056/nejmra1008153.

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15

von Schacky, Clemens. "Omega-3 fatty acids and cardiovascular disease." Current Opinion in Clinical Nutrition and Metabolic Care 10, no. 2 (March 2007): 129–35. http://dx.doi.org/10.1097/mco.0b013e3280127af0.

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16

Kris-Etherton, Penny M., William S. Harris, and Lawrence J. Appel. "Omega-3 Fatty Acids and Cardiovascular Disease." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 2 (February 2003): 151–52. http://dx.doi.org/10.1161/01.atv.0000057393.97337.ae.

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17

von Schacky, Clemens. "Omega-3 fatty acids and cardiovascular disease." Current Opinion in Clinical Nutrition and Metabolic Care 7, no. 2 (March 2004): 131–36. http://dx.doi.org/10.1097/00075197-200403000-00005.

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18

Harris, William S., and Gregory C. Shearer. "Omega-6 Fatty Acids and Cardiovascular Disease." Circulation 130, no. 18 (October 28, 2014): 1562–64. http://dx.doi.org/10.1161/circulationaha.114.012534.

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19

Westphal, Sabine, and Claus Luley. "n–3 Fatty Acids and Cardiovascular Disease." Heart Drug 2, no. 2 (2002): 83–92. http://dx.doi.org/10.1159/000063426.

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20

Nilsen, Dennis WT, and William S. Harris. "n−3 Fatty acids and cardiovascular disease." American Journal of Clinical Nutrition 79, no. 1 (January 1, 2004): 166. http://dx.doi.org/10.1093/ajcn/79.1.166.

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21

Breslow, Jan L. "n−3 Fatty acids and cardiovascular disease." American Journal of Clinical Nutrition 83, no. 6 (June 1, 2006): 1477S—1482S. http://dx.doi.org/10.1093/ajcn/83.6.1477s.

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22

Lichtenstein, Alice H. "Trans fatty acids and cardiovascular disease risk." Current Opinion in Lipidology 11, no. 1 (February 2000): 37–42. http://dx.doi.org/10.1097/00041433-200002000-00006.

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23

Sanders, Thomas A. B. "Omega-6 Fatty Acids and Cardiovascular Disease." Circulation 139, no. 21 (May 21, 2019): 2437–39. http://dx.doi.org/10.1161/circulationaha.119.040331.

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24

Mozaffarian, Dariush, and Jason H. Y. Wu. "Omega-3 Fatty Acids and Cardiovascular Disease." Journal of the American College of Cardiology 58, no. 20 (November 2011): 2047–67. http://dx.doi.org/10.1016/j.jacc.2011.06.063.

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25

Mozaffarian, Dariush. "Omega-6 fatty acids and cardiovascular disease." Nutrafoods 11, no. 3 (September 2012): 81–84. http://dx.doi.org/10.1007/s13749-012-0035-x.

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26

Fehily, Ann M. "Essential Fatty Acids and Vascular Disease." Vascular Medicine Review vmr-4, no. 4 (November 1993): 259–71. http://dx.doi.org/10.1177/1358863x9300400403.

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27

Prates, Raquel Eccel, Anize Delfino von Frankenberg, and Ticiana C. Rodrigues. "Dietary Fatty Acids and Cardiovascular Disease: A review." Clinical & Biomedical Research 35, no. 3 (2015): 126–33. http://dx.doi.org/10.4322/2357-9730.56681.

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28

Kris-Etherton, Penny M. "Monounsaturated Fatty Acids and Risk of Cardiovascular Disease." Circulation 100, no. 11 (September 14, 1999): 1253–58. http://dx.doi.org/10.1161/01.cir.100.11.1253.

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29

Willett, W. C. "Trans fatty acids and cardiovascular disease—epidemiological data." Atherosclerosis Supplements 7, no. 2 (May 2006): 5–8. http://dx.doi.org/10.1016/j.atherosclerosissup.2006.04.002.

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30

Barringer, Thomas A., and William S. Harris. "Omega-3 Fatty Acids and Cardiovascular Disease Prevention." Current Nutrition Reports 1, no. 2 (March 14, 2012): 115–22. http://dx.doi.org/10.1007/s13668-012-0011-5.

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31

DeFilippis, Andrew Paul, Michael J. Blaha, and Terry A. Jacobson. "Omega-3 Fatty Acids for Cardiovascular Disease Prevention." Current Treatment Options in Cardiovascular Medicine 12, no. 4 (May 28, 2010): 365–80. http://dx.doi.org/10.1007/s11936-010-0079-4.

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32

Singh, R. B., Fabien DeMeester, and Agnieska Wilczynska. "The Tsim Tsoum Approaches for Prevention of Cardiovascular Disease." Cardiology Research and Practice 2010 (2010): 1–18. http://dx.doi.org/10.4061/2010/824938.

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Анотація:
The Tsim Tsoum Concept means that humans evolved on a diet in which nature recommends to ingest fatty acids in a balanced ratio (polyunsaturated(P) : saturated(S) =w-6 : w-3 = 1 : 1)as part of dietary lipid pattern where monounsaturated fatty acids(MUFA) is the major fatty acid(P : M : S = 1 : 6 : 1) in the background of other dietary factors; antioxidants, vitamins, minerals and fiber as well as physical activity and low mental stress. Several hundred years ago, our diet included natural foods; fruits, vegetables, green vegetables, seeds, eggs and honey. Fish, and wild meat were also available to pre-agricultural humans which shaped modern human genetic nutritional requirement. Cereal grains (refined), and vegetable oils that are rich in w-6 fatty acids are relatively recent addition to the human diet that represent dramatic departure from those foods to which we are adapted. Excess of linoleic acid, trans fatty acids (TFA), saturated and total fat as well as refined starches and sugar are proinflammatory. Low dietary MUFA and n-3 fatty acids and other long chain polyunsarurated fatty acids (LCPUFA) are important in the pathogenesis of metabolic syndrome. Increased sympathetic activity with greater secretion of neurotransmitters in conjunction of underlying long chain PUFA deficiency, and excess of proinflammatory nutrients, may damage the neurons via proinflammatory cytokines, in the ventromedial hypothalamus and insulin receptors in the brain.Since, 30–50% of the fatty acids in the brain are LCPUFA, especially omega-3 fatty acids, which are incorporated in the cell membrane phospholipids, it is possible that their supplementation may be protective.Blood lipid composition does reflect one's health status: (a) circulating serum lipoproteins and their ratio provide information on their atherogenicity to blood vessels and (b) circulating plasma fatty acids, such as w-6/w-3 fatty acid ratio, give indication on proinflammatory status of blood vessels, cardiomyocytes, liver cells and neurones; (a) and (b) are phenotype-related and depend on genetic, environmental and developmental factors. As such, they appear as universal markers for holistic health and these may be important in the pathogenesis of cardiovascular diseases and cancer, which is the main consideration of Tsim Tsoum concept.
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33

Grenon, S. Marlene, Millie Hughes-Fulford, Joseph Rapp, and Michael S. Conte. "Polyunsaturated fatty acids and peripheral artery disease." Vascular Medicine 17, no. 1 (February 2012): 51–63. http://dx.doi.org/10.1177/1358863x11429175.

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There is substantial evidence that polyunsaturated fatty acids (PUFAs) such as n-3 and n-6 fatty acids (FAs) play an important role in prevention of atherosclerosis. In vitro and in vivo studies focusing on the interactions between monocytes and endothelial cells have explored the molecular effects of FAs on these interactions. Epidemiological surveys, followed by large, randomized, control trials have demonstrated a reduction in major cardiovascular events with supplementation of n-3 FAs in secondary prevention settings. The evidence of beneficial effects specific to patients with peripheral artery disease (PAD) remains elusive, and is the focus of this review.
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34

Harris, William S., Dariush Mozaffarian, Eric Rimm, Penny Kris-Etherton, Lawrence L. Rudel, Lawrence J. Appel, Marguerite M. Engler, Mary B. Engler, and Frank Sacks. "Omega-6 Fatty Acids and Risk for Cardiovascular Disease." Circulation 119, no. 6 (February 17, 2009): 902–7. http://dx.doi.org/10.1161/circulationaha.108.191627.

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35

Leaf, Alexander. "Health Claims: Omega-3 Fatty Acids and Cardiovascular Disease." Nutrition Reviews 50, no. 5 (April 27, 2009): 150–54. http://dx.doi.org/10.1111/j.1753-4887.1992.tb01310.x.

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36

Erkkilä, Arja, Vanessa D. F. de Mello, Ulf Risérus, and David E. Laaksonen. "Dietary fatty acids and cardiovascular disease: An epidemiological approach." Progress in Lipid Research 47, no. 3 (May 2008): 172–87. http://dx.doi.org/10.1016/j.plipres.2008.01.004.

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37

Harris, William S., Yongsoon Park, and William L. Isley. "Cardiovascular disease and long-chain omega-3 fatty acids." Current Opinion in Lipidology 14, no. 1 (February 2003): 9–14. http://dx.doi.org/10.1097/00041433-200302000-00003.

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38

Allayee, Hooman, Nitzan Roth, and Howard N. Hodis. "Polyunsaturated Fatty Acids and Cardiovascular Disease: Implications for Nutrigenetics." Journal of Nutrigenetics and Nutrigenomics 2, no. 3 (2009): 140–48. http://dx.doi.org/10.1159/000235562.

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39

Zhang, Pei-Ying. "Role of ω-3 Fatty Acids in Cardiovascular Disease". Cell Biochemistry and Biophysics 72, № 3 (7 лютого 2015): 869–75. http://dx.doi.org/10.1007/s12013-015-0554-3.

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40

De Caterina, Raffaele, and Rosalinda Madonna. "Marine n-3 Fatty Acids and Vascular Disease." Journal of the American College of Cardiology 72, no. 14 (October 2018): 1585–88. http://dx.doi.org/10.1016/j.jacc.2018.07.044.

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41

Caligiuri, Stephanie P. B., Mihir Parikh, Aleksandra Stamenkovic, Grant N. Pierce, and Harold M. Aukema. "Dietary modulation of oxylipins in cardiovascular disease and aging." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 5 (November 1, 2017): H903—H918. http://dx.doi.org/10.1152/ajpheart.00201.2017.

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Oxylipins are a group of fatty acid metabolites generated via oxygenation of polyunsaturated fatty acids and are involved in processes such as inflammation, immunity, pain, vascular tone, and coagulation. As a result, oxylipins have been implicated in many conditions characterized by these processes, including cardiovascular disease and aging. The best characterized oxylipins in relation to cardiovascular disease are derived from the ω-6 fatty acid arachidonic acid. These oxylipins generally increase inflammation, hypertension, and platelet aggregation, although not universally. Similarly, oxylipins derived from the ω-6 fatty acid linoleic acid generally have more adverse than beneficial cardiovascular effects. Alternatively, most oxylipins derived from 20- and 22-carbon ω-3 fatty acids have anti-inflammatory, antiaggregatory, and vasodilatory effects that help explain the cardioprotective effects of these fatty acids. Much less is known regarding the oxylipins derived from the 18-carbon ω-3 fatty acid α-linolenic acid, but clinical trials with flaxseed supplementation have indicated that these oxylipins can have positive effects on blood pressure. Normal aging also is associated with changes in oxylipin levels in the brain, vasculature, and other tissues, indicating that oxylipin changes with aging may be involved in age-related changes in these tissues. A small number of trials in humans and animals with interventions that contain either 18-carbon or 20- and 22-carbon ω-3 fatty acids have indicated that dietary-induced changes in oxylipins may be beneficial in slowing the changes associated with normal aging. In summary, oxylipins are an important group of molecules amenable to dietary manipulation to target cardiovascular disease and age-related degeneration.NEW & NOTEWORTHY Oxylipins are an important group of fatty acid metabolites amenable to dietary manipulation. Because of the role they play in cardiovascular disease and in age-related degeneration, oxylipins are gaining recognition as viable targets for specific dietary interventions focused on manipulating oxylipin composition to control these biological processes.
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Gerber, Philipp A., Ioanna Gouni-Berthold, and Kaspar Berneis. "Omega-3 Fatty Acids: Role in Metabolism and Cardiovascular Disease." Current Pharmaceutical Design 19, no. 17 (April 1, 2013): 3074–93. http://dx.doi.org/10.2174/1381612811319170016.

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Holub, Darren J., and Bruce J. Holub. "Omega-3 fatty acids from fish oils and cardiovascular disease." Molecular and Cellular Biochemistry 263, no. 1/2 (August 2004): 217–25. http://dx.doi.org/10.1023/b:mcbi.0000041863.11248.8d.

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Leng, G. C., G. S. Taylor, A. J. Lee, G. R. F. Fowkes, and D. Horrobin. "Essential fatty acids and cardiovascular disease: the Edinburgh Artery Study." Vascular Medicine 4, no. 4 (November 1, 1999): 219–26. http://dx.doi.org/10.1191/135886399674792102.

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Freeman, Lisa M. "Beneficial effects of omega-3 fatty acids in cardiovascular disease." Journal of Small Animal Practice 51, no. 9 (July 29, 2010): 462–70. http://dx.doi.org/10.1111/j.1748-5827.2010.00968.x.

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Saremi, Adonis, and Rohit Arora. "The Utility of Omega-3 Fatty Acids in Cardiovascular Disease." American Journal of Therapeutics 16, no. 5 (September 2009): 421–36. http://dx.doi.org/10.1097/mjt.0b013e3180a5f0bb.

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SIMOPOULOS, A. "Evolutionary aspects of diet, essential fatty acids and cardiovascular disease." European Heart Journal Supplements 3 (June 2001): D8—D21. http://dx.doi.org/10.1016/s1520-765x(01)90113-0.

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von Schacky, Clemens. "Omega-3 fatty Acids in cardiovascular disease – An uphill battle." Prostaglandins, Leukotrienes and Essential Fatty Acids 92 (January 2015): 41–47. http://dx.doi.org/10.1016/j.plefa.2014.05.004.

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Wierzbicki, A. S. "A fishy business: omega-3 fatty acids and cardiovascular disease." International Journal of Clinical Practice 62, no. 8 (July 10, 2008): 1142–46. http://dx.doi.org/10.1111/j.1742-1241.2008.01781.x.

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