Immunological mechanisms underlying sterile inflammation in the pathogenesis of atherosclerosis: potential sites for intervention

References

• Virani Salim S, Alonso A, Benjamin Emelia J, et al. Heart disease and stroke statistics—2020 update: a report from the american heart association. Circulation. 2020;141:e139–596.
   PubMed Web of Science ®Google Scholar
• Vilahur G, Badimon JJ, Bugiardini R, et al. Perspectives: the burden of cardiovascular risk factors and coronary heart disease in Europe and worldwide. Eur Heart J Suppl. 2014;16:A7–11.
   Web of Science ®Google Scholar
• Katakami N. Mechanism of development of atherosclerosis and cardiovascular disease in diabetes mellitus. J Atheroscler Thromb. 2018;25:27–39.
   PubMed Web of Science ®Google Scholar
• Hernáez Á, Soria-Florido MT, Schröder H, et al. Role of HDL function and LDL atherogenicity on cardiovascular risk: a comprehensive examination. Plos One. 2019;14:e0218533.
   PubMed Web of Science ®Google Scholar
• Hatzidakis A, Savva E, Perisinakis K, et al. CT coronary angiography in asymptomatic male patients with high atherosclerosis risk: is it justified? Hellenic J Cardiol. 2020;S110996662030066X. doi:https://doi.org/10.1016/j.hjc.2020.04.004.
   Google Scholar
• Wu M-Y, Li C-J, Hou M-F, et al. New insights into the role of inflammation in the pathogenesis of atherosclerosis. Int J Mol Sci. 2017;18:2034.
   PubMed Web of Science ®Google Scholar
• Zhang Y, Li S, Xu R-X, et al. Systemic inflammatory markers are closely associated with atherogenic lipoprotein subfractions in patients undergoing coronary angiography. Mediators Inflamm. 2015;2015:1–9.
   Web of Science ®Google Scholar
• Otsuka F, Kramer MCA, Woudstra P, et al. Natural progression of atherosclerosis from pathologic intimal thickening to late fibroatheroma in human coronary arteries: a pathology study. Atheroscler. 2015;241:772–782.
   PubMed Web of Science ®Google Scholar
• Nowak WN, Deng J, Ruan XZ, et al. Reactive oxygen species generation and atherosclerosis. Arterioscler Thromb Vasc Biol. 2017;37. doi:https://doi.org/10.1161/ATVBAHA.117.309228.
   Google Scholar
• Woollard KJ, Chin-Dusting J. Therapeutic targeting of p-selectin in atherosclerosis. Inflamm Allergy Drug Targets. 2007;6:69–74.
   PubMedGoogle Scholar
• van der Vorst EPC, Döring Y, Weber C. Chemokines and their receptors in atherosclerosis. J Mol Med. 2015;93:963–971.
   PubMed Web of Science ®Google Scholar
• Varona JF, Ortiz-Regalón R, Sánchez-Vera I, et al. Soluble ICAM 1 and VCAM 1 blood levels alert on subclinical atherosclerosis in non smokers with asymptomatic metabolic syndrome. Arch Med Res. 2019;50:20–28.
   PubMed Web of Science ®Google Scholar
• Bennett MR, Sinha S, Owens GK. Vascular smooth muscle cells in atherosclerosis. Circ Res. 2016;118:692–702.
   PubMed Web of Science ®Google Scholar
• Hasanov Z, Ruckdeschel T, König C, et al. Endosialin promotes atherosclerosis through phenotypic remodeling of vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 2017;37:495–505.
   PubMed Web of Science ®Google Scholar
• Di Pietro N, Formoso G, Pandolfi A. Physiology and pathophysiology of oxLDL uptake by vascular wall cells in atherosclerosis. Vascul Pharmacol. 2016;84:1–7.
   PubMed Web of Science ®Google Scholar
• Kattoor AJ, Goel A, Mehta JL. LOX-1: regulation, signaling and its role in atherosclerosis. Antioxid. 2019;8:218.
   Web of Science ®Google Scholar
• Burtenshaw D, Kitching M, Redmond EM, et al. Reactive oxygen species (ROS), intimal thickening, and subclinical atherosclerotic disease. Front Cardiovasc Med. 2019;6:89.
   PubMed Web of Science ®Google Scholar
• Kunjathoor VV, Febbraio M, Podrez EA, et al. Scavenger receptors class A-I/II and CD36 are the principal receptors responsible for the uptake of modified low density lipoprotein leading to lipid loading in macrophages. J Biol Chem. 2002;277:49982–49988.
   PubMed Web of Science ®Google Scholar
• Qin M, Wang L, Li F, et al. Oxidized LDL activated eosinophil polarize macrophage phenotype from M2 to M1 through activation of CD36 scavenger receptor. Atheroscler. 2017;263:82–91..
   PubMed Web of Science ®Google Scholar
• Ong S-M, Hadadi E, Dang T-M, et al. The pro-inflammatory phenotype of the human non-classical monocyte subset is attributed to senescence. Cell Death Dis. 2018;9:1–12.
   PubMed Web of Science ®Google Scholar
• Gupta Rajat M, Lee-Kim Vivian S, Libby P. The march of monocytes in atherosclerosis. Circ Res. 2020;126:1324–1326.
   PubMed Web of Science ®Google Scholar
• Wildgruber M, Aschenbrenner T, Wendorff H, et al. The “intermediate” CD14++CD16+ monocyte subset increases in severe peripheral artery disease in humans. Sci Rep. 2016;6:39483..
   PubMed Web of Science ®Google Scholar
• Ushach I, Zlotnik A. Biological role of granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) on cells of the myeloid lineage. J Leukoc Biol. 2016;100:481–489.
   PubMed Web of Science ®Google Scholar
• Costopoulos C, Huang Y, Brown AJ, et al. Plaque rupture in coronary atherosclerosis is associated with increased plaque structural stress. JACC Cardiovasc Imaging. 2017;10:1472–1483.
   PubMed Web of Science ®Google Scholar
• Lo Sasso G, Schlage WK, Boué S, et al. The apoe−/− mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction. J Transl Med. 2016;14:146.
   PubMed Web of Science ®Google Scholar
• Kimura T, Kobiyama K, Winkels H, et al. Regulatory CD4 + T cells recognize major histocompatibility complex class II molecule–restricted peptide epitopes of apolipoprotein B. Circ. 2018;138:1130–1143.
   PubMed Web of Science ®Google Scholar
• Tay C, Kanellakis P, Hosseini H, et al. B cell and CD4 T cell interactions promote development of atherosclerosis. Front Immunol. 2020;10:3046.
   PubMed Web of Science ®Google Scholar
• Wolf D, Ley K. Immunity and inflammation in atherosclerosis. Circ Res. 2019;124:315–327.
   PubMed Web of Science ®Google Scholar
• Upadhya S, Mooteri S, Peckham N, et al. Atherogenic effect of interleukin-2 and antiatherogenic effect of interleukin-2 antibody in apo-e-deficient mice. Angiology. 2016;55(3):289–294. doi:https://doi.org/10.1177/000331970405500308.
   Google Scholar
• Cole JE, Navin TJ, Cross AJ, et al. Unexpected protective role for toll-like receptor 3 in the arterial wall. Proc Natl Acad Sci. 2011;108:2372–2377.
   PubMed Web of Science ®Google Scholar
• Fang B, Ren X, Wang Y, et al. Apolipoprotein E deficiency accelerates atherosclerosis development in miniature pigs. Dis Model Mech. 2018;11:dmm036632.
   PubMed Web of Science ®Google Scholar
• Herrero-Fernandez, Gomez-Bris, Somovilla-Crespo, et al. Immunobiology of atherosclerosis: a complex net of interactions. Int J Mol Sci. 2019;20:5293.
   Web of Science ®Google Scholar
• Li J, McArdle S, Gholami A, et al. CCR5 + T-bet + FoxP3 + Effector CD4 T cells drive atherosclerosis. Circ Res. 2016;118:1540–1552.
   PubMed Web of Science ®Google Scholar
• Yasuda K, Nakanishi K, Tsutsui H. Interleukin-18 in health and disease. Int J Mol Sci. 2019;20:649.
   PubMed Web of Science ®Google Scholar
• Fatkhullina AR, Peshkova IO, Koltsova EK. The role of cytokines in the development of atherosclerosis. Biochem Mosc. 2016;81:1358–1370.
   PubMed Web of Science ®Google Scholar
• Foks AC, Kuiper J. Immune checkpoint proteins: exploring their therapeutic potential to regulate atherosclerosis. Br J Pharmacol. 2017;174:3940–3955.
   PubMed Web of Science ®Google Scholar
• Klingenberg R, Gerdes N, Badeau RM, et al. Depletion of FOXP3+ regulatory T cells promotes hypercholesterolemia and atherosclerosis. J Clin Invest. 2013;123:1323–1334.
   PubMed Web of Science ®Google Scholar
• Danzaki K, Matsui Y, Ikesue M, et al. Interleukin-17A deficiency accelerates unstable atherosclerotic plaque formation in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol. 2012;32:273–280.
   PubMed Web of Science ®Google Scholar
• Gao Q, Jiang Y, Ma T, et al. A critical function of Th17 proinflammatory cells in the development of atherosclerotic plaque in mice. J Immunol. 2010;185:5820–5827.
   PubMed Web of Science ®Google Scholar
• Gisterå A, Robertson A-KL, Andersson J, et al. Transforming growth factor–β signaling in T cells promotes stabilization of atherosclerotic plaques through an interleukin-17–dependent pathway. Sci Transl Med. 2013;5:196ra100–196ra100.
   PubMed Web of Science ®Google Scholar
• Taleb S, Romain M, Ramkhelawon B, et al. Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis. J Exp Med. 2009;206:2067–2077.
   PubMed Web of Science ®Google Scholar
• Simon T, Taleb S, Danchin N, et al. Circulating levels of interleukin-17 and cardiovascular outcomes in patients with acute myocardial infarction. Eur Heart J. 2013;34:570–577.
   PubMed Web of Science ®Google Scholar
• Madhur MS, Funt SA, Li L, et al. Role of interleukin 17 in inflammation, atherosclerosis, and vascular function in apolipoprotein E–deficient mice. Arterioscler Thromb Vasc Biol. 2011;31:1565–1572.
   PubMed Web of Science ®Google Scholar
• Ali RA, Wuescher LM, Worth RG. Platelets: essential components of the immune system. Curr Trends Immunol.  2015;16:65-78.
   Google Scholar
• Morrell CN, Aggrey AA, Chapman LM, et al. Emerging roles for platelets as immune and inflammatory cells. Blood. 2014;123:2759–2767.
   PubMed Web of Science ®Google Scholar
• Araki Y, Mimura T. The histone modification code in the pathogenesis of autoimmune diseases. Mediators Inflamm. 2017;2017:1–12.
   Web of Science ®Google Scholar
• Szatmary P, Huang W, Criddle D, et al. Biology, role and therapeutic potential of circulating histones in acute inflammatory disorders. J Cell Mol Med. 2018;22:4617–4629.
   PubMed Web of Science ®Google Scholar
• Ye X, Feng C, Gao T, et al. Linker histone in diseases. Int J Biol Sci. 2017;13:1008–1018.
   PubMed Web of Science ®Google Scholar
• Chi W, Chen H, Li F, et al. HMGB1 promotes the activation of NLRP3 and caspase-8 inflammasomes via NF-κB pathway in acute glaucoma. J Neuroinflammation. 2015;12:137.
   PubMed Web of Science ®Google Scholar
• Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev. 2018;281:8–27.
   PubMed Web of Science ®Google Scholar
• Bertheloot D, Latz E. HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins. Cell Mol Immunol. 2017;14:43–64.
   PubMed Web of Science ®Google Scholar
• Roh JS, Sohn DH. Damage-associated molecular patterns in inflammatory diseases. Immune Netw. 2018;18:e27.
   PubMed Web of Science ®Google Scholar
• Hauet-Broere F, Wieten L, Guichelaar T, et al. Heat shock proteins induce T cell regulation of chronic inflammation. Ann Rheum Dis. 2006;65:iii65–8.
   PubMed Web of Science ®Google Scholar
• Schaefer L. Complexity of danger: the diverse nature of damage-associated molecular patterns. J Biol Chem. 2014;289:35237–35245.
   PubMed Web of Science ®Google Scholar
• Srinivasan N, Gordon O, Ahrens S, et al. Actin is an evolutionarily-conserved damage-associated molecular pattern that signals tissue injury in Drosophila melanogaster. ELife. 2016;5:e19662.
   PubMed Web of Science ®Google Scholar
• Xia C, Braunstein Z, Toomey AC, et al. S100 proteins as an important regulator of macrophage inflammation. Front Immunol. 2018;8:1908.
   PubMed Web of Science ®Google Scholar
• Riley JS, Tait SW. Mitochondrial DNA in inflammation and immunity. EMBO Rep. 2020;21. DOI:https://doi.org/10.15252/embr.201949799.
   Google Scholar
• Little JP, Simtchouk S, Schindler SM, et al. Mitochondrial transcription factor a (Tfam) is a pro-inflammatory extracellular signaling molecule recognized by brain microglia. Mol Cell Neurosci. 2014;60:88–96.
   PubMed Web of Science ®Google Scholar
• Volobueva A, Grechko A, Yet S-F, et al. Changes in mitochondrial genome associated with predisposition to atherosclerosis and related disease. Biomolecules. 2019;9:377.
   Web of Science ®Google Scholar
• Fornai F. The inflammatory protein pentraxin 3 in cardiovascular disease. 2016;13(1):25. doi: https://doi.org/10.1186/s12979-016-0080-1.
   Google Scholar
• Norata GD, Marchesi P, Pulakazhi Venu VK, et al. Deficiency of the long pentraxin PTX3 promotes vascular inflammation and atherosclerosis. Circ. 2009;120:699–708.
   PubMed Web of Science ®Google Scholar
• Zindel J, Kubes P. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation. Annu Rev Pathol Mech Dis. 2020;15:493–518.
   PubMed Web of Science ®Google Scholar
• Magna M, Pisetsky DS. The role of HMGB1 in the pathogenesis of inflammatory and autoimmune diseases. Mol Med. 2014;20:138–146.
   PubMed Web of Science ®Google Scholar
• Lu B, Wang H, Andersson U, et al. Regulation of HMGB1 release by inflammasomes. Protein Cell. 2013;4:163–167.
   PubMed Web of Science ®Google Scholar
• Andersson U, Tracey KJ. HMGB1 is a therapeutic target for sterile inflammation and infection. Annu Rev Immunol. 2011;29:139–162.
   PubMed Web of Science ®Google Scholar
• Wang B, Wei G, Liu B, et al. The role of high mobility group box 1 protein in interleukin-18-induced myofibroblastic transition of valvular interstitial cells. Cardiol. 2016;135:168–178.
   PubMed Web of Science ®Google Scholar
• Schmidt AM. 2016 ATVB plenary lecture: receptor for advanced glycation endproducts and implications for the pathogenesis and treatment of cardiometabolic disorders: spotlight on the macrophage. Arterioscler Thromb Vasc Biol. 2017;37:613–621. .
   PubMed Web of Science ®Google Scholar
• Fiuza C, Bustin M, Talwar S, et al. Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. Blood. 2003;101:2652–2660.
   PubMed Web of Science ®Google Scholar
• Yang H, Wang H, Czura CJ, et al. The cytokine activity of HMGB1. J Leukoc Biol. 2005;78:1–8.
   PubMed Web of Science ®Google Scholar
• Edfeldt K, Swedenborg J, Hansson GK, et al. Expression of toll-like receptors in human atherosclerotic lesions: a possible pathway for plaque activation. Circulation. 2002;105:1158–1161.
   PubMed Web of Science ®Google Scholar
• Ott C, Jacobs K, Haucke E, et al. Role of advanced glycation end products in cellular signaling. Redox Biol. 2014;2:411–429.
   PubMed Web of Science ®Google Scholar
• Shi D, Chang JW, Choi J, et al. Receptor for advanced glycation end products (RAGE) is expressed predominantly in medium spiny neurons of tgHD rat striatum. Neuroscience. 2018;380:146–151.
   PubMed Web of Science ®Google Scholar
• Fritz G. RAGE: a single receptor fits multiple ligands. Trends Biochem Sci. 2011;36:625–632.
   PubMed Web of Science ®Google Scholar
• Chen Y-J, Chan D-C, Chiang C-K, et al. Advanced glycation end-products induced VEGF production and inflammatory responses in human synoviocytes via RAGE-NF-κB pathway activation. J Orthop Res. 2016;34:791–800.
   PubMed Web of Science ®Google Scholar
• Senatus LM, Schmidt AM, The AGE, et al. Implications for age-associated arterial diseases. Front Genet. 2017;8. doi:https://doi.org/10.3389/fgene.2017.00187
   Google Scholar
• Zhong H, Li X, Zhou S, et al. Interplay between RAGE and TLR4 regulates HMGB1-induced inflammation by promoting cell surface expression of RAGE and TLR4. J Immunol. 2020. doi:https://doi.org/10.4049/jimmunol.1900860.
   Google Scholar
• Yang H, Hreggvidsdottir HS, Palmblad K, et al. A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release. Proc Natl Acad Sci. 2010;107:11942–11947.
   PubMed Web of Science ®Google Scholar
• Björkbacka H, Kunjathoor VV, Moore KJ, et al. Reduced atherosclerosis in MyD88-null mice links elevated serum cholesterol levels to activation of innate immunity signaling pathways. Nat Med. 2004;10:416–421.
   PubMed Web of Science ®Google Scholar
• Chandrashekaran V, Seth RK, Dattaroy D, et al. HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease. Redox Biol. 2017;13:8–19.
   PubMed Web of Science ®Google Scholar
• Roshan MHK, Tambo A, Pace NP. The role of TLR2, TLR4, and TLR9 in the pathogenesis of atherosclerosis. Int J Inflamm. 2016;2016:1–11.
   Web of Science ®Google Scholar
• Michelsen KS, Wong MH, Shah PK, et al. Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E. Proc Natl Acad Sci. 2004;101:10679–10684.
   PubMed Web of Science ®Google Scholar
• Chen T, Luo W, Wu G, et al. A novel MyD88 inhibitor LM9 prevents atherosclerosis by regulating inflammatory responses and oxidative stress in macrophages. Toxicol Appl Pharmacol. 2019;370:44–55.
   PubMed Web of Science ®Google Scholar
• Yin Y-W, Liao S-Q, Zhang M-J, et al. TLR4-mediated inflammation promotes foam cell formation of vascular smooth muscle cell by upregulating ACAT1 expression. Cell Death Dis. 2014;5:e1574–e1574.
   PubMed Web of Science ®Google Scholar
• Gargiulo S, Gamba P, Testa G, et al. Relation between TLR4/NF-κB signaling pathway activation by 27-hydroxycholesterol and 4-hydroxynonenal, and atherosclerotic plaque instability. Aging Cell. 2015;14:569–581.
   PubMed Web of Science ®Google Scholar
• Yang H, Lundbäck P, Ottosson L, et al. Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1). Mol Med. 2012;18:250–259.
   PubMed Web of Science ®Google Scholar
• Yang H, Wang H, Ju Z, et al. MD-2 is required for disulfide HMGB1–dependent TLR4 signaling. J Exp Med. 2015;212:5–14..
   PubMed Web of Science ®Google Scholar
• Gliozzi M, Scicchitano M, Bosco F, et al. Modulation of nitric oxide synthases by oxidized LDLs: role in vascular inflammation and atherosclerosis development. Int J Mol Sci. 2019;20:3294.
   Web of Science ®Google Scholar
• Lin F, Pei L, Zhang Q, et al. Ox-LDL induces endothelial cell apoptosis and macrophage migration by regulating caveolin-1 phosphorylation. J Cell Physiol. 2018;233:6683–6692.
   PubMed Web of Science ®Google Scholar
• Cai J, Yuan H, Wang Q, et al. HMGB1-driven inflammation and intimal hyperplasia after arterial injury involves cell-specific actions mediated by TLR4. Arterioscler Thromb Vasc Biol. 2015;35:2579–2593.
   PubMed Web of Science ®Google Scholar
• Sims GP, Rowe DC, Rietdijk ST, et al. HMGB1 and RAGE in inflammation and cancer. Annu Rev Immunol. 2010;28:367–388.
   PubMed Web of Science ®Google Scholar
• Cao X, Zhang L, Chen C, et al. The critical role of ABCG1 and PPARγ/LXRα signaling in TLR4 mediates inflammatory responses and lipid accumulation in vascular smooth muscle cells. Cell Tissue Res. 2017;368:145–157.
   PubMed Web of Science ®Google Scholar
• Lake NJ, Taylor RL, Trahair H, et al. TRAK2, a novel regulator of ABCA1 expression, cholesterol efflux and HDL biogenesis. Eur Heart J. 2017;38:3579–3587.
   PubMed Web of Science ®Google Scholar
• Nakaya K, Tohyama J, Naik SU, et al. Peroxisome proliferator-activated receptor-α activation promotes macrophage reverse cholesterol transport through a liver X receptor–dependent pathway. Arterioscler Thromb Vasc Biol. 2011;31:1276–1282.
   PubMed Web of Science ®Google Scholar
• Rohatgi A, Khera A, Berry JD, et al. HDL cholesterol efflux capacity and incident cardiovascular events. N Engl J Med. 2014;371:2383–2393.
   PubMed Web of Science ®Google Scholar
• Mullick AE, Soldau K, Kiosses WB, et al. Increased endothelial expression of Toll-like receptor 2 at sites of disturbed blood flow exacerbates early atherogenic events. J Exp Med. 2008;205:373–383.
   PubMed Web of Science ®Google Scholar
• Liu X, Ukai T, Yumoto H, et al. Toll-like receptor 2 plays a critical role in the progression of atherosclerosis that is independent of dietary lipids. Atheroscler. 2008;196:146–154.
   PubMed Web of Science ®Google Scholar
• Rangasamy SB, Jana M, Roy A, et al. Selective disruption of TLR2-MyD88 interaction inhibits inflammation and attenuates Alzheimer’s pathology. J Clin Invest. 2018;128:4297–4312.
   PubMed Web of Science ®Google Scholar
• Lee G-L, Chang Y-W, Wu J-Y, et al. TLR 2 induces vascular smooth muscle cell migration through camp response element−binding protein−mediated interleukin-6 production. Arterioscler Thromb Vasc Biol. 2012;32:2751–2760.
   PubMed Web of Science ®Google Scholar
• Yokoi H, Yanagita M. Targeting the fatty acid transport protein CD36, a class B scavenger receptor, in the treatment of renal disease. Kidney Int. 2016;89:740–742.
   PubMed Web of Science ®Google Scholar
• Xiao X, Yang C, Qu S-L, et al. S100 proteins in atherosclerosis. Clin Chim Acta. 2020;502:293–304.
   PubMed Web of Science ®Google Scholar
• Oesterle A, Bowman MAH. S100A12 and the S100/calgranulins - emerging biomarkers for atherosclerosis and possibly therapeutic targets. 2015;35(12):2496-507. doi:https://doi.org/10.1161/ATVBAHA.115.302072.
   Google Scholar
• Ligthart S, Sedaghat S, Ikram MA, et al. EN-RAGE: a novel inflammatory marker for incident coronary heart disease. Arterioscler Thromb Vasc Biol. 2014;34:2695–2699.
   PubMed Web of Science ®Google Scholar
• Averill MM, Kerkhoff C, Bornfeldt KE. S100A8 and S100A9 in cardiovascular biology and disease. Arterioscler Thromb Vasc Biol. 2012;32:223–229.
   PubMed Web of Science ®Google Scholar
• Croce K, Gao H, Wang Y, et al. Myeloid-related protein-8/14 is critical for the biological response to vascular injury. Circ. 2009;120:427–436.
   PubMed Web of Science ®Google Scholar
• Ellsworth DL, Croft DT, Weyandt J, et al. Intensive cardiovascular risk reduction induces sustainable changes in expression of genes and pathways important to vascular function. Circ Cardiovasc Genet. 2014;7:151–160.
   PubMedGoogle Scholar
• Gawdzik J, Mathew L, Kim G, et al. Vascular remodeling and arterial calcification are directly mediated by S100A12 (EN-RAGE) in chronic kidney disease. Am J Nephrol. 2011;33:250–259.
   PubMed Web of Science ®Google Scholar
• Sun J, Sukhova GK, Wolters PJ, et al. Mast cells promote atherosclerosis by releasing proinflammatory cytokines. Nat Med. 2007;13:719–724.
   PubMed Web of Science ®Google Scholar
• Farokhzadian J, Mangolian Shahrbabaki P, Bagheri VS. 100A12-CD36 axis: A novel player in the pathogenesis of atherosclerosis? Cytokine. 2019;122:154104.
   PubMed Web of Science ®Google Scholar
• Tondera C, Laube M, Pietzsch J. Insights into binding of S100 proteins to scavenger receptors: class B scavenger receptor CD36 binds S100A12 with high affinity. Amino Acids. 2017;49:183–191.
   PubMed Web of Science ®Google Scholar
• Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140:805–820.
   PubMed Web of Science ®Google Scholar
• Lamkanfi M, Dixit VM. Inflammasomes and their roles in health and disease. Annu Rev Cell Dev Biol. 2012;28:137–161.
   PubMed Web of Science ®Google Scholar
• Zeng C, Wang R, Tan H. Role of pyroptosis in cardiovascular diseases and its therapeutic implications. Int J Biol Sci. 2019;15:1345–1357.
   PubMed Web of Science ®Google Scholar
• Lamkanfi M, Dixit VM. Mechanisms and functions of inflammasomes. Cell. 2014;157:1013–1022. .
   PubMed Web of Science ®Google Scholar
• Bruchard M, Rebé C, Derangère V, et al. The receptor NLRP3 is a transcriptional regulator of T H 2 differentiation. Nat Immunol. 2015;16:859–870.
   PubMed Web of Science ®Google Scholar
• Baldrighi M, Mallat Z, Li X. NLRP3 inflammasome pathways in atherosclerosis. Atheroscler. 2017;267:127–138.
   PubMed Web of Science ®Google Scholar
• Muñoz-Planillo R, Kuffa P, Martínez-Colón G, et al. K+ efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immun. 2013;38:1142–1153.
   Google Scholar
• Chevriaux A, Pilot T, Derangère V, et al. Cathepsin B is required for NLRP3 inflammasome activation in macrophages, through NLRP3 interaction. Front Cell Dev Biol. 2020;8. doi:https://doi.org/10.3389/fcell.2020.00167.
   Google Scholar
• Shimada K. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. Immunity. 2012;36(3):401-14. doi: https://doi.org/10.1016/j.immuni.2012.01.009.
   Google Scholar
• Kim EJ, Park SY, Baek SE, et al. HMGB1 increases IL-1β production in vascular smooth muscle cells via NLRP3 inflammasome. Front Physiol. 2018;9:313..
   PubMed Web of Science ®Google Scholar
• Wang R, Wu W, Li W, et al. Activation of NLRP3 inflammasome promotes foam cell formation in vascular smooth muscle cells and atherogenesis via HMGB1. J Am Heart Assoc. 2018;7. doi:https://doi.org/10.1161/JAHA.118.008596.
   Google Scholar
• Eun SY, Ko YS, Park SW, et al. IL-1β enhances vascular smooth muscle cell proliferation and migration via P2Y2 receptor-mediated RAGE expression and HMGB1 release. Vascul Pharmacol. 2015;72:108–117.
   PubMed Web of Science ®Google Scholar
• Sheedy FJ, Grebe A, Rayner KJ, et al. CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation. Nat Immunol. 2013;14:812–820..
   PubMed Web of Science ®Google Scholar
• Stewart CR, Stuart LM, Wilkinson K, et al. CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer. Nat Immunol. 2010;11:155–161..
   PubMed Web of Science ®Google Scholar
• Paramel Varghese G, Folkersen L, Strawbridge RJ, et al. NLRP3 inflammasome expression and activation in human atherosclerosis. J Am Heart Assoc. 2016;5. doi:https://doi.org/10.1161/JAHA.115.003031.
   Google Scholar
• Getz GS, Reardon CA. Do the Apoe −/− and Ldlr −/– mice yield the same insight on atherogenesis? Arterioscler Thromb Vasc Biol. 2016;36:1734–1741.
   PubMed Web of Science ®Google Scholar
• Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464:1357–1361.
   PubMed Web of Science ®Google Scholar
• Hendrikx T, Jeurissen MLJ, Gorp PJV, et al. Bone marrow-specific caspase-1/11 deficiency inhibits atherosclerosis development in Ldlr−/ − mice. Febs J. 2015;282:2327–2338.
   PubMed Web of Science ®Google Scholar
• Menu P, Pellegrin M, Aubert J-F, et al. Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome. Cell Death Dis. 2011;2:e137–e137.
   PubMed Web of Science ®Google Scholar
• Shi X, Xie W-L, Kong -W-W, et al. Expression of the NLRP3 inflammasome in carotid atherosclerosis. J Stroke Cerebrovasc Dis. 2015;24:2455–2466.
   PubMed Web of Science ®Google Scholar
• Ding J, Wang K, Liu W, et al. Pore-forming activity and structural autoinhibition of the gasdermin family. Nature. 2016;535:111–116.
   PubMed Web of Science ®Google Scholar
• Liu X, Zhang Z, Ruan J, et al. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. Nature. 2016;535:153–158.
   PubMed Web of Science ®Google Scholar
• Sborgi L, Rühl S, Mulvihill E, et al. GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death. Embo J. 2016;35:1766–1778.
   PubMed Web of Science ®Google Scholar
• Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017;377:1119–1131.
   PubMed Web of Science ®Google Scholar
• Charles‐Schoeman C, Yin Lee Y, Shahbazian A, et al. Improvement of high-density lipoprotein function in patients with early rheumatoid arthritis treated with methotrexate monotherapy or combination therapies in a randomized controlled trial. Arthritis Rheumatol. 2017;69(1):46–57.
   PubMed Web of Science ®Google Scholar
• Reiss AB, Carsons SE, Anwar K, et al. Atheroprotective effects of methotrexate on reverse cholesterol transport proteins and foam cell transformation in human THP-1 monocyte/macrophages. Arthritis Rheum. 2008;58:3675–3683.
   PubMed Web of Science ®Google Scholar
• Ridker PM, Everett BM, Pradhan A, et al. Low-dose methotrexate for the prevention of atherosclerotic events. N Engl J Med. 2019;380:752–762.
   PubMed Web of Science ®Google Scholar
• Ma C, Wang Y, Dong L, et al. Anti-inflammatory effect of resveratrol through the suppression of NF- B and JAK/STAT signaling pathways. Acta Biochim Biophys Sin. 2015;47:207–213.
   Google Scholar
• Lu B, Antoine DJ, Kwan K, et al. JAK/STAT1 signaling promotes HMGB1 hyperacetylation and nuclear translocation. Proc Natl Acad Sci. 2014;111:3068–3073.
   PubMed Web of Science ®Google Scholar
• Irey EA, Lassiter CM, Brady NJ, et al. JAK/STAT inhibition in macrophages promotes therapeutic resistance by inducing expression of protumorigenic factors. Proc Natl Acad Sci. 2019;116:12442–12451.
   PubMed Web of Science ®Google Scholar
• Yang H, Wang H, Chavan SS, et al. High mobility group box protein 1 (HMGB1): the prototypical endogenous danger molecule. Mol Med. 2015;21:S6–12.
   PubMed Web of Science ®Google Scholar
• Sun S, He M, Wang Y, et al. Folic acid derived-P5779 mimetics regulate DAMP-mediated inflammation through disruption of HMGB1:TLR4:MD-2 axes. Plos One. 2018;13:e0193028.
   PubMed Web of Science ®Google Scholar
• Zhou F, Tan Y. Atorvastatin improves plaque stability in diabetic atherosclerosis through the RAGE pathway. Eur Rev Med Pharmacol Sci. 2018;22(4):1142-1149. doi:https://doi.org/10.26355/eurrev_201802_14403.
   Google Scholar
• Peng S, Xu L-W, Che X-Y, et al. Atorvastatin inhibits inflammatory response, attenuates lipid deposition, and improves the stability of vulnerable atherosclerotic plaques by modulating autophagy. Front Pharmacol. 2018;9:438.
   PubMed Web of Science ®Google Scholar
• Cao L, Pan D, Li D, et al. Relation between anti-atherosclerotic effects of IRAK4 and modulation of vascular smooth muscle cell phenotype in diabetic rats. Am J Transl Res. 2016;8(2):899-910.
   Google Scholar
• Singer JW, Fleischman A, Al-Fayoumi S, et al. Inhibition of interleukin-1 receptor-associated kinase 1 (IRAK1) as a therapeutic strategy. Oncotarget. 2018;9:33416–33439.
   PubMedGoogle Scholar
• Seijkens TTP, van Tiel CM, Kusters PJH, et al. Targeting CD40-induced TRAF6 signaling in macrophages reduces atherosclerosis. J Am Coll Cardiol. 2018;71:527–542.
   PubMed Web of Science ®Google Scholar
• Gareus R, Kotsaki E, Xanthoulea S, et al. Endothelial cell-specific NF-κB inhibition protects mice from atherosclerosis. Cell Metab. 2008;8:372–383.
   PubMed Web of Science ®Google Scholar
• Paciolla M, Pescatore A, Conte MI, et al. Rare mendelian primary immunodeficiency diseases associated with impaired NF-κB signaling. Genes Immun. 2015;16:239–246.
   PubMed Web of Science ®Google Scholar
• Rathkey JK, Zhao J, Liu Z, et al. Chemical disruption of the pyroptotic pore-forming protein gasdermin D inhibits inflammatory cell death and sepsis. Sci Immunol. 2018;3:eaat2738.
   PubMed Web of Science ®Google Scholar
• Xing -S-S, Yang J, Li W, et al. Salidroside decreases atherosclerosis plaque formation via inhibiting endothelial cell pyroptosis. Inflammation. 2020;43:433–440.
   PubMed Web of Science ®Google Scholar