Церамиды: взаимосвязь с факторами риска сердечно-сосудистых заболеваний

Автор: Е.В. Белик, Ю.А. Дылева, О.В. Груздева

Журнал: Сибирский журнал клинической и экспериментальной медицины @cardiotomsk

Статья в выпуске: 1 т.38, 2023 года.

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Несмотря на достигнутые успехи, ведущей причиной смертности во всем мире остаются сердечно-сосудистые заболевания (ССЗ). С помощью традиционных факторов риска не всегда возможно выявить всех пациентов с высокой вероятностью развития сердечно-сосудистых событий (CCC), поэтому до сих пор остается актуальной проблема поиска новых биомаркеров ССЗ. Ранее проведенные исследования показали важную роль избыточного синтеза церамидов в развитии ожирения, инсулинорезистентности (ИР), сахарного диабета 2-го типа (СД2), стеатоза печени. Считается, что церамиды способны модулировать сигнальные пути, участвующие в регуляции метаболизма глюкозы, синтеза триацилглицеролов (ТАГ), развитии апоптоза, фиброза и атеросклероза. Учитывая широкий спектр метаболических эффектов, изучение церамидов является перспективным для выявления пациентов высокого риска ССЗ и улучшения существующих лечебно-диагностических стратегий. В этой обзорной статье рассмотрена роль церамидов в развитии атеросклероза, взаимосвязь с традиционными факторами риска, а также возможность их использования в качестве новых факторов риска для ранней диагностики ССЗ.

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Церамиды, факторы риска, сердечно-сосудистые заболевания, курение

Короткий адрес: https://sciup.org/149141578

IDR: 149141578 | DOI: 10.29001/2073-8552-2023-38-1-28-36

Список литературы Церамиды: взаимосвязь с факторами риска сердечно-сосудистых заболеваний

Шрамко В.С., Морозов С.В., Черняк Е.И., Щербакова Л.В., Кургузов А.В., Чернявский А.М. и др. Клинические характеристики пациентов с атеросклерозом коронарных артерий в зависимости от жирно-кислотного спектра крови. Комплексные проблемы сердечно-сосудистых заболеваний. 2020;9(1):15–24. [Shramko V.S., Morozov S.V., Chernyak E.I., Shcherbakova L.V., Kurguzov A.V., Chernyavskyi A.M. et al. Clinical characteristics of patients with coronary atherosclerosis depending on blood fatty acids. Complex Issues of Cardiovascular Diseases. 2020;9(1):15–24. (In Russ.)]. DOI: 10.17802/2306-1278-2020-9-1-15-24.
Carrard J., Gallart-Ayala H., Weber N., Colledge F., Streese L., Hanssen H. et al. How ceramides orchestrate cardiometabolic health-an ode to physically active living. Metabolites. 2021;11(10):675. DOI: 10.3390/metabo11100675.
Kuijpers P. History in medicine: The story of cholesterol, lipids and cardiology. J. Cradiol. Pract. 2021;19:1–5.
Laaksonen R., Ekroos K., Sysi-Aho M., Hilvo M., Vihervaara T., Kauhanen D. et al. Plasma ceramides predict cardiovascular death in patients with stable coronary artery disease and acute coronary syndromes beyond LDL-cholesterol. Eur. Heart J. 2016;37:1967–1976. DOI: 10.1093/eurheartj/ehw148.
Hilvo M., Meikle P.J., Pedersen E.R., Tell G.S., Dhar I., Brenner H. et al. Development and validation of a ceramide- and phospholipid-based cardiovascular risk estimation score for coronary artery disease patients. Eur. Heart. J. 2019;41:371–380. DOI: 10.1093/eurheartj/ehz387.
Meeusen J.W., Donato L.J., Bryant S.C., Baudhuin L.M., Berger P.B., Jaffe A.S. et al. Plasma Ceramides: A novel predictor of major adverse cardiovascular events after coronary angiography. Arterioscler. Thromb. Vasc. Biol. 2018;38(8):1933–1939. DOI: 10.1161/atvbaha.118.311199.
Shalaby Y.M., Al Aidaros A., Valappil A., Ali B.R., Akawi N. Role of Ceramides in the molecular pathogenesis and potential therapeutic strategies of cardiometabolic diseases: What we know so far. Front. Cell Dev. Biol. 2022;9:816301. DOI: 10.3389/fcell.2021.816301.
Yang F., Liu C., Liu X., Pan X., Li X., Tian L. et al. Effect of epidemic intermittent fasting on cardiometabolic risk factors: A systematic review and meta-analysis of randomized controlled trials. Front. Nutr. 2021;8:669325. DOI: 10.3389/fnut.2021.669325.
Havulinna A.S., Sysi-Aho M., Hilvo M., Kauhanen D., Hurme R., Ekroos K. et al. Circulating ceramides predict cardiovascular outcomes in the population- based FINRISK 2002 Cohort. Arterioscler. Thromb. Vasc. Biol. 2016;36(12):2424–2430. DOI: 10.1161/ATVBAHA.116.307497.
Vasile V.C., Meeusen J.W., Inojosa M.J.R., Donato L.J., Scott C.G., Hyun M.S. et al. Ceramide scores predict cardiovascular risk in the community. Arterioscler. Thromb. Vasc. Biol. 2021;41(4):1558–1569. DOI: 10.1161/ATVBAHA.120.315530.
Chatham J.C., Young M.E. Metabolic remodeling in the hypertrophic heart: fuel for thought. Circ. Res. 2012;111:666–668. DOI: 10.1161/circresaha.112.277392.
Merrill A.H.Jr. Sphingolipid and glycosphingolipid metabolic pathways in the era of sphingolipidomics. Chemistry Review. 2011;111:6387–6422. DOI: 10.1021/cr2002917.
Tippetts T.S., Holland W.L., Summers S.A. Cholesterol – the devil you know; ceramide – the devil you don’t. Trends. Pharmacol. Sci. 2021;42(12):1082–1095. DOI: 10.1016/j.tips.2021.10.001.
McGurk K.A., Keavney B.D., Nicolaou A. Circulating ceramides as biomarkers of cardiovascular disease: Evidence from phenotypic and genomic studies. Atherosclerosis. 2021;327:18–30. DOI: 10.1016/j.atherosclerosis.2021.04.021.
Crewe C., Joffi N., Rutkowski J.M., Kim M., Zhang F., Towler D.A. et al. An endothelial-to-adipocyte extracellular vesicle axis governed by metabolic state. An. Cell. 2018;175(3):695–708.e13. DOI: 10.1016/j.cell.2018.09.005.
Li W., Yang X., Xing S., Bian F., Yao W., Bai X. et al. Endogenous ceramide contributes to the transcytosis of oxldl across endothelial cells and promotes its subendothelial retention in vascular wall. Oxid. Med. Cell Longev. 2014;823071. DOI: 10.1155/2014/823071.
Ruuth M., Nguyen S.D., Vihervaara T., Hilvo M., Laajala T.D., Kondadi P.K. et al. Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths. Eur. Heart J. 2018;39(27):2562–2573. DOI: 10.1093/eurheartj/ehy319.
Ichi I., Nakahara K., Miyashita Y., Hidaka A., Kutsukake S., Inoue K. et al. Association of ceramides in human plasma with risk factors of atherosclerosis. Lipids. 2006;41(9):859–863. DOI: 10.1007/s11745-006-5041-6.
Ng T.W., Ooi E.M., Watts G.F., Chan D.C., Meikle P.J., Barrett P.H. Association of plasma ceramides and sphingomyelin with VLDL apoB-100 fractional catabolic rate before and after rosuvastatin treatment. J. Clin. Endocrinol. Metab. 2015;100(6):2497–2501. DOI: 10.1210/jc.2014-4348.
Zhou B., Xiao J.F., Tuli L., Ressom H.W. LC-MS-based metabolomics. Mol. Biosyst. 2012;8(2):470–481. DOI: 10.1039/c1mb05350g.
Kita Y., Tokuoka S.M., Shimizu T. Mediator lipidomics by liquid chromatography- tandem mass spectrometry. Biochim. Biophys. Acta Mol. Cell. Biol. Lipids. 2017;1862(8):777–781. DOI: 10.1016/j.bbalip.2017.03.008.
Lange M., Angelidou G., Ni Z., Criscuolo A., Schiller J., Blüher M. et al. AdipoAtlas: A reference lipidome for human white adipose tissue. Cell Rep. Med. 2021;2(10):100407. DOI: 10.1016/j.xcrm.2021.100407.
Hojjati M.R., Li Z., Zhou H., Tang S., Huan C., Ooi E. et al. Effect of myriocin on plasma sphingolipid metabolism and atherosclerosis in apoE-deficient mice. J. Biol. Chem. 2005;280:10284–10289. DOI: 10.1074/jbc.M412348200.
Meikle P.J., Wong G., Tsorotes D., Barlow C.K., Weir J.M., Christopher M.J. et al. Plasma lipidomic analysis of stable and unstable coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 2011;31(11):2723–2732. DOI: 10.1161/ATVBAHA.111.234096.
Alonso A., Goñi F.M. The Physical Properties of Ceramides in Membranes. Annu Rev. Biophys. 2018;47:633–654. DOI: 10.1146/annurev-biophys-070317-033309.
Fretts A.M., Jensen P.N., Hoofnagle A.N., McKnight B., Sitlani C.M., Siscovick D.S. et al. Circulating ceramides and sphingomyelins and risk of mortality: The cardiovascular health study. Clin. Chem. 2021;67:1650–1659. DOI: 10.1093/clinchem/hvab182.
Anroedh S., Hilvo M., Akkerhuis K.M., Kauhanen D., Koistinen K., Oemrawsingh R. et al. Plasma concentrations of molecular lipid species predict long-term clinical outcome in coronary artery disease patients. J. Lipid Res. 2018;59:1729–1737. DOI: 10.1194/jlr.P081281.
Mundra P.A., Barlow C.K., Nestel P.J., Barnes E.H., Kirby A., Thompson P. et al. Large-scale plasma lipidomic profiling identifies lipids that predict cardiovascular events in secondary prevention. JCI Insight.2018;3:121326. DOI: 10.1172/jci.insight.121326.
Hilvo M., Wallentin L., Ghukasyan Lakic T., Held C., Kauhanen D., Jylhä A. et al. Prediction of residual risk by ceramide-phospholipid score in patients with stable coronary heart disease on optimal medical therapy.J. Am. Heart. Assoc. 2020;9:e015258. DOI: 10.1161/JAHA.119.015258.
SCORE2 working group and ESC Cardiovascular risk collaboration. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe. Eur. Heart J. 2021;42(25):2439–2454. DOI: 10.1093/eurheartj/ehab309.
Poss A.M., Maschek J.A., Cox J.E., Hauner B.J., Hopkins P.N., Hunt S.C. et al. Machine learning reveals serum sphingolipids as cholesterol-independent biomarkers of coronary artery disease. J. Clin. Invest. 2020;130(3):1363–1376. DOI: 10.1172/JCI131838.
Wagner-Golbs A., Neuber S., Kamlage B., Christiansen N., Bethan B., Rennefahrt U. et al. Effects of long-term storage at -80°C on the human plasma metabolome. Metabolites. 2019;9(5):99. DOI: 10.3390/metabo9050099.
Walls S.M., Cammarato A., Chatfield D.A., Ocorr K., Harris G.L., Bodmer R. Ceramide-protein interactions modulate ceramide-associated lipotoxic cardiomyopathy. Cell Rep. 2018;22:2702–2715. DOI: 10.1016/j.celrep.2018.02.034.
Kurz J., Parnham M.J., Geisslinger G., Schiffmann S. Ceramides as novel disease biomarkers. Trends Molecular Medicine. 2019;25(1):20–32. DOI: 10.1016/j.molmed.2018.10.009.
Vozella V., Basit A., Piras F., Realini N., Armirotti A., Bossù P. et al. Elevated plasma ceramide levels in post-menopausal women: A cross-sectional study. Aging. 2019;11(1):73–88. DOI: 10.18632/aging.101719.
Mielke M.M., Bandaru V.V.R., Han D., An Y., Resnick S.M., Ferrucci L. et al. Demographic and clinical variables affecting mid- to late-life trajectories of plasma ceramide and dihydroceramide species. Aging Cell. 2015;14:1014–1023. DOI: 10.1111/acel.12369.
Wooten-Blanks L.G., Song P., Senkal C.E., Ogretmen B. Mechanisms of ceramide-mediated repression of the human telomerase reverse transcriptase promoter via deacetylation of Sp3 by histone deacetylase 1. Faseb. J. 2007;21:3386–3397. DOI: 10.1096/fj.07-8621com.
Smith A.R., Visioli F., Frei B., Hagen T.M. Age-related changes in endothelial nitric oxide synthase phosphorylation and nitric oxide dependent vasodilation: evidence for a novel mechanism involving sphingomyelinase and ceramide-activated phosphatase 2A. Aging Cell. 2006;5(5):391–400. DOI: 10.1111/j.1474-9726.2006.00232.x.
Mielke M.M., Bandaru V.V.R., Han D., An Y., Resnick S.M., Ferrucci L. et al. Factors affecting longitudinal trajectories of plasma sphingomyelins: Baltimore Longitudinal Study of Aging. Aging Cell. 2015;14:112–121. DOI: 10.1111/acel.12275.
Bui H.H., Leohr J.K., Kuo M.S. Analysis of sphingolipids in extracted human plasma using liquid chromatography electrospray ionization tandem mass spectrometry. Anal. Biochem. 2012;423(2):187–194. DOI: 10.1016/j.ab.2012.01.027.
Hammad S.M., Pierce J.S., Soodavar F., Smith K.J., Al Gadban M.M., Rembiesa B. et al. Blood sphingolipidomics in healthy humans: impact of sample collection methodology. J. Lipid Res. 2010;51(10):3074–3087. DOI: 10.1194/jlr.D008532.
Jeyarajah E.J., Cromwell W.C., Otvos J.D. Lipoprotein particle analysis by nuclear magnetic resonance spectroscopy. Clin. Lab. Med. 2006;26:847–870. DOI: 10.1016/j.cll.2006.07.006.
Di Palo K.E., Barone N.J. Hypertension and heart failure: prevention, targets, and treatment. Heart Fail. Clin. 2020;16:99–106. DOI: 10.1016/j.hfc.2019.09.001.
Spijkers L.J., van den Akker R.F., Janssen B.J., Debets J.J., De Mey J.G., Stroes E.S. et al. Hypertension is associated with marked alterations in sphingolipid biology: a potential role for ceramide. PLoS One. 2011;6(7):e21817. DOI: 10.1371/journal.pone.0021817.
Lin Y.-T., Salihovic S., Fall T., Hammar U., Ingelsson E., Ärnlöv J. et al. Global plasma metabolomics to identify potential biomarkers of blood pressure progression. Arterioscler. Thromb. Vasc. Biol. 2020;40:e227–e237. DOI: 10.1161/ATVBAHA.120.314356.
Kulkarni H., Meikle P.J., Mamtani M., Weir J.M., Barlow C.K., Jowett J.B. et al. Plasma lipidomic profi le signature of hypertension in Mexican American families: specifi c role of diacylglycerols. Hypertension. 2013;62(3):621–626. DOI: 10.1161/HYPERTENSIONAHA.113.01396.
Spijkers L.J., Janssen B.J., Nelissen J., Meens M.J., Wijesinghe D., Chalfant C.E. Antihypertensive treatment diff erentially aff ects vascular sphingolipid biology in spontaneously hypertensive rats. PLoS One. 2011;6(12):e29222. DOI: 10.1371/journal.pone.0029222.
Liu A., Chu Y.-J., Wang X., Yu R., Jiang H., Li Y. et al. Serum metabolomics study based on LC-MS and antihypertensive eff ect of uncaria on spontaneously hypertensive rats. Evid. Based Complement. Alternat. Med. 2018;2018:9281946. DOI: 10.1155/2018/9281946.
van den Elsen L.W., Spijkers L.J., van den Akker R.F., van Winssen A.M., Balvers M., Wijesinghe D.S. Dietary fi sh oil improves endothelial function and lowers blood pressure via suppression of sphingolipid-mediated contractions in spontaneously hypertensive rats. J. Hypertens. 2014;32(5):1050–1058; discussion 1058. DOI: 10.1097/HJH.0000000000000131.
Chaurasia B., Summers S.A. Ceramides-Lipotoxic inducers of metabolic disorders. Trends Endocrinol. Metab. 2015;26:538–550. DOI: 10.1016/j.tem.2015.07.006.
Poss A.M., Summers S.A. Too much of a good thing? An evolutionary theory to explain the role of ceramides in nafl d. Front. Endocrinol. 2020;11:505. DOI: 10.3389/fendo.2020.00505.
Summers S.A., Chaurasia B., Holland W.L. Metabolic messengers: Ceramides. Nat. Metab. 2019;1(11):1051–1058. DOI: 10.1038/s42255-019-0134-8.
Raichur S., Wang S.T., Chan P.W., Li Y., Ching J., Chaurasia B. et al. CerS2 haploinsuffi ciency inhibits β-Oxidation and confers susceptibility to diet-induced steatohepatitis and insulin resistance. Cell Metab. 2014;20(4):687–695. DOI: 10.1016/j.cmet.2014.09.015.
Vijay A., Astbury S., Panayiotis L., Marques F.Z., Spector T.D., Menni C. et al. Dietary interventions reduce traditional and novel cardiovascular risk markers by altering the gut microbiome and their metabolites. Front. Cardiovasc. Med. 2021;8:691564. DOI: 10.3389/fcvm.2021.691564.
Hilvo M., Simolin H., Metso J., Ruuth M., Öörni K., Jauhiainen M. et al. PCSK9 inhibition alters the lipidome of plasma and lipoprotein fractions. Atherosclerosis. 2018;269:159–165. DOI: 10.1016/j.atherosclerosis.2018.01.004.
Aittokallio J., Palmu J., Niiranen T. Smoking is the strongest modifi able risk factor for mortality post coronary revascularisation. Eur. J. Prev. Cardiol. 2020;27:2308–2310. DOI: 10.1177/2047487319894883.
Parasuraman S., Zaman A.G., Egred M., Bagnall A., Broadhurst P.A., Ahmed J. et al. Smoking status and mortality outcomes following percutaneous coronary intervention. Eur. J. Prev. Cardiol. 2020;28:1222–1228. DOI: 10.1177/2047487320902325.
Boué S., Tarasov K., Jänis M., Lebrun S., Hurme R., Schlage W. et al. Modulation of atherogenic lipidome by cigarette smoke in apolipoprotein E-defi cient mice. Atherosclerosis. 2012;225(2):328–334. DOI: 10.1016/j.atherosclerosis.2012.09.032.
Cruickshank-Quinn C.I., Mahaff ey S., Justice M.J., Hughes G., Armstrong M., Bowler R.P. et al. Transient and persistent metabolomics changes in plasma following chronic cigarette smoke exposure in a mouse model. PLoS One. 2014;9(7):e101855. DOI: 10.1371/journal.pone.0101855.
Lavrynenko O., Titz B., Dijon S., Santos D.D., Nury C., Schneider T. et al. Ceramide ratios are aff ected by cigarette smoke but not heat-not-burn or e-vapor aerosols across four independent mouse studies. Life Sci. 2020;263:118753. DOI: 10.1016/j.lfs.2020.118753.

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