[1] BHATT D L, LOPES R D, HARRINGTON R A. Diagnosis and treatment of acute coronary syndromes: a review[J]. JAMA, 2022, 327(7): 662-675. [2] LIBBY P, PASTERKAMP G, CREA F, et al. Reassessing the mechanisms of acute coronary syndromes[J]. Circ Res, 2019,124(1): 150-160. [3] FAHED A C, JANG I K. Plaque erosion and acute coronary syndromes: phenotype, molecular characteristics and future directions[J]. Nat Rev Cardiol, 2021,18(10): 724-734. [4] PRADHAN A D, ADAY A W, ROSE L M, et al. Residual inflammatory risk on treatment with PCSK9 inhibition and statin therapy[J]. Circulation, 2018, 138(2): 141-149. [5] NADEL J, JABBOUR A, STOCKER R. Arterial myeloperoxidase in the detection and treatment of vulnerable atherosclerotic plaque: a new dawn for an old light[J]. Cardiovasc Res, 2023, 119(1): 112-120. [6] TAN Y, YANG S, CHEN R, et al. High plasma myeloperoxidase is associated with plaque erosion in patients with ST-segment elevation myocardial infarction[J]. J Cardiovasc Transl Res, 2020, 13(6): 908-915. [7] CHENG D, TALIB J, STANLEY C P, et al. Inhibition of MPO (Myeloperoxidase) attenuates endothelial dysfunction in mouse models of vascular inflammation and atherosclerosis[J]. Arterioscler Thromb Vasc Biol, 2019,39(7): 1448-1457. [8] CHEN W, TUMANOV S, KONG S, et al. Therapeutic inhibition of MPO stabilizes pre-existing high risk atherosclerotic plaque[J]. Redox Biol, 2022, 10(58): 25-32. [9] ZHANG G, QIN Q, ZHANG C, et al. NDRG1 signaling is essential for endothelial inflammation and vascular remodeling [J]. Circ Res, 2023, 132(3): 306-319. [10] KIM H O, JIANG B, POON E, et al. High endothelial shear stress and stress gradient at plaque erosion persist up to 12 months[J]. Int J Cardiol, 2022, 357: 1-7. [11] YAMAMOTO E, THONDAPU V, POON E, et al. Endothelial shear stress and plaque erosion: a computational fluid dynamics and optical coherence tomography study[J]. JACC Cardiovasc Imaging, 2019, 12(2): 374-375. [12] MARTINOD K, WAGNER D D. Thrombosis: tangled up in NETs[J]. Blood, 2014, 123(18): 2768-2776. [13] FOLCO E J, MAWSON T L, VROMMAN A, et al. Neutrophil extracellular traps induce endothelial cell activation and tissue factor production through interleukin-1alpha and cathepsin G[J]. Arterioscler Thromb Vasc Biol, 2018,38(8): 1901-1912. [14] MA Y, YANG X, CHATTERJEE V, et al. Role of neutrophil extracellular traps and vesicles in regulating vascular endothelial permeability[J]. Front Immunol, 2019,10: 1037-1046. [15] BLANCH-RUIZ M A, ORTEGA-LUNA R, MARTINEZ-CUESTA M A, et al. The neutrophil secretome as a crucial link between inflammation and thrombosis[J]. Int J Mol Sci, 2021, 22(8) :4170-4191. [16] FRANCK G, MAWSON T L, FOLCO E J, et al. Roles of PAD4 and NETosis in experimental atherosclerosis and arterial injury: implications for superficial erosion[J]. Circ Res, 2018, 123(1): 33-42. [17] MOLINARO R, YU M, SAUSEN G, et al. Targeted delivery of protein arginine deiminase-4 inhibitors to limit arterial intimal NETosis and preserve endothelial integrity[J]. Cardiovasc Res, 2021, 117(13): 2652-2663. [18] DU M, YANG W, SCHMULL S, et al. Inhibition of peptidyl arginine deiminase-4 protects against myocardial infarction induced cardiac dysfunction[J]. Int Immunopharmacol, 2020,78: 106055. [19] LIU J, YANG D, WANG X, et al. Neutrophil extracellular traps and dsDNA predict outcomes among patients with ST-elevation myocardial infarction[J]. Sci Rep, 2019,9(1): 11599. [20] PERTIWI K R, DE BOER O J, MACKAAIJ C, et al. Extracellular traps derived from macrophages, mast cells, eosinophils and neutrophils are generated in a time-dependent manner during atherothrombosis[J]. J Pathol, 2019, 247(4): 505-512. [21] SINGH P, KUMAR N, SINGH M, et al. Neutrophil extracellular traps and NLRP3 inflammasome: a disturbing duo in atherosclerosis, inflammation and atherothrombosis[J]. Vaccines: Basel, 2023, 11(2):261-275. [22] RIDKER P M, EVERETT B M, THUREN T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease[J]. N Engl J Med, 2017, 377(12): 1119-1131. [23] NIDORF S M, FIOLET A, MOSTERD A, et al. Colchicine in patients with chronic coronary disease[J]. N Engl J Med, 2020, 383(19): 1838-1847. [24] OPSTAL T, FIOLET A, VAN BROEKHOVEN A, et al. Colchicine in patients with chronic coronary disease in relation to prior acute coronary syndrome[J]. J Am Coll Cardiol, 2021, 78(9): 859-866. [25] OPSTAL T, VAN BROEKHOVEN A, FIOLET A, et al. Long-term efficacy of colchicine in patients with chronic coronary disease: insights from LoDoCo2[J]. Circulation, 2022, 145(8): 626-628. [26] WEI K, HUANG H, LIU M, et al. Platelet-derived exosomes and atherothrombosis[J]. Front Cardiovasc Med, 2022, 9: 886132. [27] KURAVI S J, HARRISON P, RAINGER G E, et al. Ability of platelet-derived extracellular vesicles to promote neutrophil-endothelial cell interactions[J]. Inflammation, 2019, 42(1): 290-305. [28] GABA P, GERSH B J, MULLER J, et al. Evolving concepts of the vulnerable atherosclerotic plaque and the vulnerable patient: implications for patient care and future research[J]. Nat Rev Cardiol, 2023, 20(3): 181-196. [29] GERHARDT T, SEPPELT C, ABDELWAHED Y S, et al. Culprit plaque morphology determines inflammatory risk and clinical outcomes in acute coronary syndrome[J]. Eur Heart J, 2023, 44(38):3911-3925. |