Abstract
Cardiovascular diseases (CVDs) are the foremost cause of mortality worldwide. Atherosclerosis is the underlying pathology behind CVDs. Atherosclerosis is manifested predominantly by lipid deposition, plaque formation, and inflammation in vascular intima. Initiation and progression of plaque require many years. With aging, atherosclerotic plaques become vulnerable. Localization of these plaques in the coronary artery leads to myocardial infarction. A complete understanding of the pathophysiology of this multifaceted disease is necessary to achieve the clinical goal to provide early diagnosis and the best therapeutics. The triggering factors of atherosclerosis are biomechanical forces, hyperlipidemia, and chronic inflammatory response. The current review focuses on crucial determinants involved in the disease, such as location, hemodynamic factors, oxidation of low-density lipoproteins, and the role of endothelial cells, vascular smooth muscle cells, and immune cells, and better therapeutic targets.
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References
Wang S, Ren J (2018) Obesity paradox in aging: from prevalence to pathophysiology. Prog Cardiovasc Dis 61:182–189. https://doi.org/10.1016/j.pcad.2018.07.011
Curtiss LK (2009) Reversing atherosclerosis? N Engl J Med 360:1144–1146. https://doi.org/10.1056/NEJMcibr0810383
Morbiducci U, Kok AM, Kwak BR et al (2016) Atherosclerosis at arterial bifurcations: evidence for the role of haemodynamics and geometry. Thromb Haemost 115:484–492. https://doi.org/10.1160/TH15-07-0597
Kwak BR, Bäck M, Bochaton-Piallat M-L et al (2014) Biomechanical factors in atherosclerosis: mechanisms and clinical implications. Eur Heart J 35:3013–3020. https://doi.org/10.1093/eurheartj/ehu353
Phan TG, Beare RJ, Jolley D et al (2012) Carotid artery anatomy and geometry as risk factors for carotid atherosclerotic disease. Stroke 43:1596–1601. https://doi.org/10.1161/STROKEAHA.111.645499
Warboys C (2011) The role of blood flow in determining the sites of atherosclerotic plaques. F1000 Medicine Reports 3:. https://doi.org/10.3410/M3-5
Lu D, Kassab GS (2011) Role of shear stress and stretch in vascular mechanobiology. J R Soc Interface 8:1379–1385. https://doi.org/10.1098/rsif.2011.0177
Cheng C (2005) Shear stress affects the intracellular distribution of eNOS: direct demonstration by a novel in vivo technique. Blood 106:3691–3698. https://doi.org/10.1182/blood-2005-06-2326
Dhawan SS, Avati Nanjundappa RP, Branch JR et al (2010) Shear stress and plaque development. Expert Rev Cardiovasc Ther 8:545–556. https://doi.org/10.1586/erc.10.28
Versluis A, Bank AJ, Douglas WH (2006) Fatigue and plaque rupture in myocardial infarction. J Biomech 39:339–347. https://doi.org/10.1016/j.jbiomech.2004.10.041
Brooks AR, Lelkes PI, Rubanyi GM (2002) Gene expression profiling of human aortic endothelial cells exposed to disturbed flow and steady laminar flow. Physiol Genomics 9:27–41. https://doi.org/10.1152/physiolgenomics.00075.2001
Yang J, Cho K, Kim J et al (2014) Wall shear stress in hypertensive patients is associated with carotid vascular deformation assessed by speckle tracking strain imaging. Clinical Hypertension 20:10. https://doi.org/10.1186/2056-5909-20-10
Brown AJ, Teng Z, Evans PC et al (2016) Role of biomechanical forces in the natural history of coronary atherosclerosis. Nat Rev Cardiol 13:210–220. https://doi.org/10.1038/nrcardio.2015.203
Sakakura K, Nakano M, Otsuka F et al (2013) Pathophysiology of atherosclerosis plaque progression. Heart Lung Circ 22:399–411. https://doi.org/10.1016/j.hlc.2013.03.001
Meydani M (2001) Vitamin E and atherosclerosis: beyond prevention of LDL oxidation. J Nutr 131:366S-368S
Dugas TR, Morel DW, Harrison EH (1998) Impact of LDL carotenoid and alpha-tocopherol content on LDL oxidation by endothelial cells in culture. J Lipid Res 39:999–1007
Hevonoja T, Pentikäinen MO, Hyvönen MT, et al (2000) Structure of low density lipoprotein (LDL) particles: Basis for understanding molecular changes in modified LDL. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1488:189–210. https://doi.org/10.1016/S1388-1981(00)00123-2
Itabe H (2009) Oxidative modification of LDL: its pathological role in atherosclerosis. Clinic Rev Allerg Immunol 37:4–11. https://doi.org/10.1007/s12016-008-8095-9
Fogelstrand P, Borén J (2016) Catch and release: NG2-coated vascular smooth muscle cells capture lipoproteins for macrophages. Arterioscler Thromb Vasc Biol 36:7–8. https://doi.org/10.1161/ATVBAHA.115.306798
Mundi S, Massaro M, Scoditti E et al (2018) Endothelial permeability, LDL deposition, and cardiovascular risk factors—a review. Cardiovasc Res 114:35–52. https://doi.org/10.1093/cvr/cvx226
Yoshida H, Kisugi R (2010) Mechanisms of LDL oxidation. Clin Chim Acta 411:1875–1882. https://doi.org/10.1016/j.cca.2010.08.038
Parthasarathy S, Raghavamenon A, Garelnabi MO, Santanam N (2010) Oxidized low-density lipoprotein. In: Uppu RM, Murthy SN, Pryor WA, Parinandi NL (eds) Free radicals and antioxidant protocols. Humana Press, Totowa, NJ, pp 403–417
Arai H, Berlett BS, Chock PB, Stadtman ER (2005) Effect of bicarbonate on iron-mediated oxidation of low-density lipoprotein. PNAS 102:10472–10477. https://doi.org/10.1073/pnas.0504685102
Satchell L, Leake DS (2012) Oxidation of low-density lipoprotein by iron at lysosomal pH: implications for atherosclerosis. Biochemistry 51:3767–3775. https://doi.org/10.1021/bi2017975
Steinberg D (1997) Low density lipoprotein oxidation and its pathobiological significance. J Biol Chem 272:20963–20966. https://doi.org/10.1074/jbc.272.34.20963
Moore KJ, Tabas I (2011) Macrophages in the pathogenesis of atherosclerosis. Cell 145:341–355. https://doi.org/10.1016/j.cell.2011.04.005
Maingrette F, Renier G (2005) Linoleic Acid Increases Lectin-Like Oxidized LDL Receptor-1 (LOX-1) expression in human aortic endothelial cells. Diabetes 54:1506–1513. https://doi.org/10.2337/diabetes.54.5.1506
Thakkar S, Wang X, Khaidakov M et al (2015) Structure-based design targeted at LOX-1, a receptor for oxidized low-density lipoprotein. Sci Rep. https://doi.org/10.1038/srep16740
Chistiakov DA, Melnichenko AA, Myasoedova VA et al (2017) Mechanisms of foam cell formation in atherosclerosis. J Mol Med 95:1153–1165. https://doi.org/10.1007/s00109-017-1575-8
Parks BW, Lusis AJ (2013) Macrophage accumulation in atherosclerosis. N Engl J Med 369:2352–2353. https://doi.org/10.1056/NEJMcibr1312709
Robbins CS, Hilgendorf I, Weber GF et al (2013) Local proliferation dominates lesional macrophage accumulation in atherosclerosis. Nat Med 19:1166–1172. https://doi.org/10.1038/nm.3258
Ghattas A, Griffiths HR, Devitt A et al (2013) Monocytes in coronary artery disease and atherosclerosis: where are we now? J Am Coll Cardiol 62:1541–1551. https://doi.org/10.1016/j.jacc.2013.07.043
Jaipersad AS, Lip GYH, Silverman S, Shantsila E (2014) The role of monocytes in angiogenesis and atherosclerosis. J Am Coll Cardiol 63:1–11. https://doi.org/10.1016/j.jacc.2013.09.019
Rocha VZ, Libby P (2009) Obesity, inflammation, and atherosclerosis. Nat Rev Cardiol 6:399–409. https://doi.org/10.1038/nrcardio.2009.55
Ouimet M, Marcel YL (2012) Regulation of lipid droplet cholesterol efflux from macrophage foam cells. Arterioscler Thromb Vasc Biol 32:575–581. https://doi.org/10.1161/ATVBAHA.111.240705
Glass CK, Witztum JL (2001) Atherosclerosis. the road ahead. Cell 104:503–516
Sekiya M, Osuga J-I, Igarashi M et al (2011) The role of neutral cholesterol ester hydrolysis in macrophage foam cells. J Atheroscler Thromb 18:359–364
Ghosh S (2012) Early steps in reverse cholesterol transport: cholesteryl ester hydrolase and other hydrolases. Curr Opinion Endocrinol Diabetes Obesity 19:136–141. https://doi.org/10.1097/MED.0b013e3283507836
Yuan Y, Li P, Ye J (2012) Lipid homeostasis and the formation of macrophage-derived foam cells in atherosclerosis. Protein Cell 3:173–181. https://doi.org/10.1007/s13238-012-2025-6
Trogan E, Feig JE, Dogan S et al (2006) Gene expression changes in foam cells and the role of chemokine receptor CCR7 during atherosclerosis regression in ApoE-deficient mice. Proc Natl Acad Sci 103:3781–3786. https://doi.org/10.1073/pnas.0511043103
Gerszten RE, Tager AM (2012) The monocyte in atherosclerosis—should I stay or should I go now? N Engl J Med 366:1734–1736. https://doi.org/10.1056/NEJMcibr1200164
Mudau M, Genis A, Lochner A, Strijdom H (2012) Endothelial dysfunction : the early predictor of atherosclerosis. Cardiovasc J Afr 23:222–231. https://doi.org/10.5830/CVJA-2011-068
Tabas I, García-Cardeña G, Owens GK (2015) Recent insights into the cellular biology of atherosclerosis. J Cell Biol 209:13–22. https://doi.org/10.1083/jcb.201412052
Cunningham KS, Gotlieb AI (2005) The role of shear stress in the pathogenesis of atherosclerosis. Lab Invest 85:9–23. https://doi.org/10.1038/labinvest.3700215
Hofmann A, Brunssen C, Poitz DM et al (2017) Lectin-like oxidized low-density lipoprotein receptor-1 promotes endothelial dysfunction in LDL receptor knockout background. Atheroscler Suppl 30:294–302. https://doi.org/10.1016/j.atherosclerosissup.2017.05.020
Gimbrone MA, García-Cardeña G (2016) Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circ Res 118:620–636. https://doi.org/10.1161/CIRCRESAHA.115.306301
Davignon J (2004) Role of endothelial dysfunction in atherosclerosis. Circulation. https://doi.org/10.1161/01.CIR.0000131515.03336.f8
Evrard SM, Lecce L, Michelis KC et al (2016) Endothelial to mesenchymal transition is common in atherosclerotic lesions and is associated with plaque instability. Nat Commun 7:11853. https://doi.org/10.1038/ncomms11853
Chen P-Y, Qin L, Baeyens N et al (2015) Endothelial-to-mesenchymal transition drives atherosclerosis progression. J Clin Investig 125:4514–4528. https://doi.org/10.1172/JCI82719
Bennett MR, Sinha S, Owens GK (2016) Vascular smooth muscle cells in atherosclerosis. Circ Res 118:692–702. https://doi.org/10.1161/CIRCRESAHA.115.306361
Newby A (2006) Matrix metalloproteinases regulate migration, proliferation, and death of vascular smooth muscle cells by degrading matrix and non-matrix substrates. Cardiovasc Res 69:614–624. https://doi.org/10.1016/j.cardiores.2005.08.002
Ketelhuth DFJ, Bäck M (2011) The role of matrix metalloproteinases in atherothrombosis. Curr Atheroscler Rep 13:162–169. https://doi.org/10.1007/s11883-010-0159-7
Ushakumary MG, Wang M, V H, et al (2019) Discoidin domain Receptor 2: A determinant of metabolic syndrome-associated arterial fibrosis in non-human primates. PLoS ONE 14:e0225911. https://doi.org/10.1371/journal.pone.0225911
Maiellaro K, Taylor W (2007) The role of the adventitia in vascular inflammation. Cardiovasc Res 75:640–648. https://doi.org/10.1016/j.cardiores.2007.06.023
Benditt EP (1977) The origin of atherosclerosis. Sci Am 236:74–85
Ferrara N, Gerber H-P, LeCouter J (2003) The biology of VEGF and its receptors. Nat Med 9:669–676. https://doi.org/10.1038/nm0603-669
al GM et Segmental heterogeneity of vasa vasorum neovascularization in human coronary atherosclerosis. - PubMed - NCBI. https://www.ncbi.nlm.nih.gov/pubmed/20129528/. Accessed 26 Nov 2017
Gössl M, Versari D, Mannheim D et al (2007) Increased spatial vasa vasorum density in the proximal LAD in hypercholesterolemia—Implications for vulnerable plaque-development. Atherosclerosis 192:246–252. https://doi.org/10.1016/j.atherosclerosis.2006.07.004
Parma L, Baganha F, Quax PHA, de Vries MR (2017) Plaque angiogenesis and intraplaque hemorrhage in atherosclerosis. Eur J Pharmacol 816:107–115. https://doi.org/10.1016/j.ejphar.2017.04.028
Badimon L, Vilahur G (2014) Thrombosis formation on atherosclerotic lesions and plaque rupture. J Intern Med 276:618–632. https://doi.org/10.1111/joim.12296
Bakogiannis C, Sachse M, Stamatelopoulos K, Stellos K (2017) Platelet-derived chemokines in inflammation and atherosclerosis. Cytokine. https://doi.org/10.1016/j.cyto.2017.09.013
Camera M, Brambilla M, Facchinetti L et al (2012) Tissue Factor and Atherosclerosis: Not only vessel wall-derived TF, but also platelet-associated TF. Thromb Res 129:279–284. https://doi.org/10.1016/j.thromres.2011.11.028
Costopoulos C, Huang Y, Brown AJ et al (2017) Plaque rupture in coronary atherosclerosis is associated with increased plaque structural stress. JACC Cardiovasc Imag. https://doi.org/10.1016/j.jcmg.2017.04.017
Lee JM, Choi G, Hwang D et al (2017) Impact of longitudinal lesion geometry on location of plaque rupture and clinical presentations. JACC Cardiovasc Imaging 10:677–688. https://doi.org/10.1016/j.jcmg.2016.04.012
Pagiatakis C, Galaz R, Tardif J-C, Mongrain R (2015) A comparison between the principal stress direction and collagen fiber orientation in coronary atherosclerotic plaque fibrous caps. Med Biol Eng Compu 53:545–555. https://doi.org/10.1007/s11517-015-1257-z
Lee K, Santibanez-Koref M, Polvikoski T et al (2013) Increased expression of fatty acid binding protein 4 and leptin in resident macrophages characterises atherosclerotic plaque rupture. Atherosclerosis 226:74–81. https://doi.org/10.1016/j.atherosclerosis.2012.09.037
Vergallo R, Crea F (2020) Atherosclerotic plaque healing. N Engl J Med 383:846–857. https://doi.org/10.1056/NEJMra2000317
Vergallo R, Porto I, D’Amario D et al (2019) Coronary atherosclerotic phenotype and plaque healing in patients with recurrent acute coronary syndromes compared with patients with long-term clinical stability: an in vivo optical coherence tomography study. JAMA Cardiol 4:321. https://doi.org/10.1001/jamacardio.2019.0275
Koren MJ, Jones PH, Robinson JG et al (2020) A comparison of ezetimibe and evolocumab for atherogenic lipid reduction in four patient populations: a pooled efficacy and safety analysis of three phase 3 studies. Cardiol Ther 9:447–465. https://doi.org/10.1007/s40119-020-00181-8
Jeries H, Volkova N, Grajeda-Iglesias C et al (2020) Prednisone and its active metabolite prednisolone attenuate lipid accumulation in macrophages. J Cardiovasc Pharmacol Ther 25:174–186. https://doi.org/10.1177/1074248419883591
Ma J, Chen X (2021) Anti-inflammatory therapy for coronary atherosclerotic heart disease: unanswered questions behind existing successes. Front Cardiovasc Med 7:631398. https://doi.org/10.3389/fcvm.2020.631398
Pillai SC, Borah A, Jacob EM, Kumar DS (2021) Nanotechnological approach to delivering nutraceuticals as promising drug candidates for the treatment of atherosclerosis. Drug Delivery 28:550–568. https://doi.org/10.1080/10717544.2021.1892241
Ahmad F, Mitchell RD, Houben T et al (2021) Cysteamine decreases low-density lipoprotein oxidation, causes regression of atherosclerosis, and improves liver and muscle function in low-density lipoprotein receptor-deficient mice. JAHA. https://doi.org/10.1161/JAHA.120.017524
Gupta KK, Ali S, Sanghera RS (2019) Pharmacological options in atherosclerosis: a review of the existing evidence. Cardiol Ther 8:5–20. https://doi.org/10.1007/s40119-018-0123-0
Bäck M, Hansson GK (2015) Anti-inflammatory therapies for atherosclerosis. Nat Rev Cardiol 12:199–211. https://doi.org/10.1038/nrcardio.2015.5
Olszowy-Tomczyk M (2020) Synergistic, antagonistic and additive antioxidant effects in the binary mixtures. Phytochem Rev 19:63–103. https://doi.org/10.1007/s11101-019-09658-4
Dasagrandhi D, R ASK, Muthuswamy A, et al (2018) Ischemia/reperfusion injury in male guinea pigs: An efficient model to investigate myocardial damage in cardiovascular complications. Biomed Pharmacother 99:469–479. https://doi.org/10.1016/j.biopha.2018.01.087
Ridker PM, Everett BM, Thuren T et al (2017) Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 377:1119–1131. https://doi.org/10.1056/NEJMoa1707914
Yang J, Zhang L, Yu C et al (2014) Monocyte and macrophage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases. Biomarker Research 2:1. https://doi.org/10.1186/2050-7771-2-1
Idzkowska E, Eljaszewicz A, Miklasz P et al (2015) The role of different monocyte subsets in the pathogenesis of atherosclerosis and acute coronary syndromes. Scand J Immunol 82:163–173. https://doi.org/10.1111/sji.12314
Wildgruber M, Aschenbrenner T, Wendorff H et al (2016) The “Intermediate” CD14++CD16+ monocyte subset increases in severe peripheral artery disease in humans. Sci Rep. https://doi.org/10.1038/srep39483
Stansfield BK, Ingram DA (2015) Clinical significance of monocyte heterogeneity. Clin Transl Med. https://doi.org/10.1186/s40169-014-0040-3
Cros J, Cagnard N, Woollard K et al (2010) Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors. Immunity 33:375–386. https://doi.org/10.1016/j.immuni.2010.08.012
Thomas G, Tacke R, Hedrick CC, Hanna RN (2015) Nonclassical patrolling monocyte function in the vasculature. Arterioscler Thromb Vasc Biol 35:1306–1316. https://doi.org/10.1161/ATVBAHA.114.304650
Chinetti-Gbaguidi G, Colin S, Staels B (2015) Macrophage subsets in atherosclerosis. Nat Rev Cardiol 12:10–17. https://doi.org/10.1038/nrcardio.2014.173
Colin S, Chinetti-Gbaguidi G, Staels B (2014) Macrophage phenotypes in atherosclerosis. Immunol Rev 262:153–166. https://doi.org/10.1111/imr.12218
Wilson HM (2010) Macrophages heterogeneity in atherosclerosis - implications for therapy. J Cell Mol Med 14:2055–2065. https://doi.org/10.1111/j.1582-4934.2010.01121.x
Gui T, Shimokado A, Sun Y et al (2012) Diverse roles of macrophages in atherosclerosis: from inflammatory biology to biomarker discovery. Mediators Inflamm. https://doi.org/10.1155/2012/693083
Bobryshev YV, Ivanova EA, Chistiakov DA et al (2016) Macrophages and their role in atherosclerosis: pathophysiology and transcriptome analysis. Biomed Res Int. https://doi.org/10.1155/2016/9582430
Vinchi F, Muckenthaler MU, Da Silva MC et al (2014) Atherogenesis and iron: from epidemiology to cellular level. Front Pharmacol. https://doi.org/10.3389/fphar.2014.00094
Tse K, Tse H, Sidney J et al (2013) T cells in atherosclerosis. Int Immunol 25:615–622. https://doi.org/10.1093/intimm/dxt043
Okada R, Kondo T, Matsuki F et al (2008) Phenotypic classification of human CD4+ T cell subsets and their differentiation. Int Immunol 20:1189–1199. https://doi.org/10.1093/intimm/dxn075
Ammirati E, Moroni F, Magnoni M, Camici PG (2015) The role of T and B cells in human atherosclerosis and atherothrombosis. Clin Exp Immunol 179:173–187. https://doi.org/10.1111/cei.12477
Iwata H, Manabe I, Nagai R (2013) Lineage of bone marrow-derived cells in atherosclerosis. Circ Res 112:1634–1647. https://doi.org/10.1161/circresaha.113.301384
Chistiakov DA, Orekhov AN, Bobryshev YV (2016) Immune-inflammatory responses in atherosclerosis: Role of an adaptive immunity mainly driven by T and B cells. Immunobiology 221:1014–1033. https://doi.org/10.1016/j.imbio.2016.05.010
Brucklacher-Waldert V, Steinbach K, Lioznov M et al (2009) Phenotypical characterization of human Th17 cells unambiguously identified by surface IL-17A expression. J Immunol 183:5494–5501. https://doi.org/10.4049/jimmunol.0901000
Gotsman I, Sharpe AH, Lichtman AH (2008) T-cell costimulation and coinhibition in atherosclerosis. Circ Res 103:1220–1231. https://doi.org/10.1161/CIRCRESAHA.108.182428
Dietel B, Cicha I, Voskens CJ et al (2013) Decreased numbers of regulatory T cells are associated with human atherosclerotic lesion vulnerability and inversely correlate with infiltrated mature dendritic cells. Atherosclerosis 230:92–99. https://doi.org/10.1016/j.atherosclerosis.2013.06.014
Zhuang J, Han Y, Xu D et al (2017) Comparison of circulating dendritic cell and monocyte subsets at different stages of atherosclerosis: insights from optical coherence tomography. BMC Cardiovasc Disord 17:270. https://doi.org/10.1186/s12872-017-0702-3
Daissormont ITMN, Christ A, Temmerman L et al (2011) Plasmacytoid dendritic cells protect against atherosclerosis by tuning T-cell proliferation and activity. Circ Res 109:1387–1395. https://doi.org/10.1161/CIRCRESAHA.111.256529
Chistiakov DA, Sobenin IA, Orekhov AN, Bobryshev YV (2015) Myeloid dendritic cells: Development, functions, and role in atherosclerotic inflammation. Immunobiology 220:833–844. https://doi.org/10.1016/j.imbio.2014.12.010
Selathurai A, Deswaerte V, Kanellakis P et al (2014) Natural killer (NK) cells augment atherosclerosis by cytotoxic-dependent mechanisms. Cardiovasc Res 102:128–137. https://doi.org/10.1093/cvr/cvu016
van Puijvelde G, van Wanrooij E, Hauer A et al (2009) Effect of natural killer T cell activation on initiation of atherosclerosis. Thromb Haemost 102:223–230. https://doi.org/10.1160/TH09-01-0020
Montaldo E, Zotto GD, Chiesa MD et al (2013) Human NK cell receptors/markers: A tool to analyze NK cell development, subsets and function: Human NK Cell Receptors/Markers. Cytometry A 83A:702–713. https://doi.org/10.1002/cyto.a.22302
Ionita MG, van den Borne P, Catanzariti LM et al (2010) High neutrophil numbers in human carotid atherosclerotic plaques are associated with characteristics of rupture-prone lesions. Arterioscler Thromb Vasc Biol 30:1842–1848. https://doi.org/10.1161/ATVBAHA.110.209296
Getz GS, Reardon CA (2017) Natural killer T cells in atherosclerosis. Nat Rev Cardiol 14:304–314. https://doi.org/10.1038/nrcardio.2017.2
Sun J, Sukhova GK, Wolters PJ et al (2007) Mast cells promote atherosclerosis by releasing proinflammatory cytokines. Nat Med 13:719–724. https://doi.org/10.1038/nm1601
Smith DD, Tan X, Raveendran VV et al (2012) Mast cell deficiency attenuates progression of atherosclerosis and hepatic steatosis in apolipoprotein E-null mice. Am J Physiol-Heart Circulatory Physiol 302:H2612–H2621. https://doi.org/10.1152/ajpheart.00879.2011
Li Y (2001) Mast cells/basophils in the peripheral blood of allergic individuals who are HIV-1 susceptible due to their surface expression of CD4 and the chemokine receptors CCR3, CCR5, and CXCR4. Blood 97:3484–3490. https://doi.org/10.1182/blood.V97.11.3484
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This work was financially supported by the Food and Nutrition project, Department of Biotechnology, India: Grant BT/PR6327/FNS/20/606/2012. ICMR Grant No: 2019-2605/CMB/Adhoc-BMS ; RUSA 2.0, Biologicals Sciences, Bharathidasan University, India.
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Divya Dasagrandhi has conceptualized, did the literature search, and has written the first draft of the manuscript. Anusuyadevi Muthuswamy provided valuable suggestions and corrected the manuscript. Jayachandran Kesavan Swaminathan added valuable suggestions, and monitored and corrected the manuscript.
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Dasagrandhi, D., Muthuswamy, A. & Swaminathan, J.K. Atherosclerosis: nexus of vascular dynamics and cellular cross talks. Mol Cell Biochem 477, 571–584 (2022). https://doi.org/10.1007/s11010-021-04307-x
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DOI: https://doi.org/10.1007/s11010-021-04307-x