参考文献/References:
[1]Borissoff JI,Joosen IA,Versteylen MO,et al. Elevated levels of circulating DNA and chromatin are independently associated with severe coronary atherosclerosis and a prothrombotic state[J]. Arterioscler Thromb Vasc Biol,2013,33(8):2032-2040.
[2]Gimbrone MA Jr,García-Carde?a G. Endothelial cell dysfunction and the pathobiology of atherosclerosis[J]. Circ Res,2016,118(4):620-636.
[3]Ramji DP,Davies TS. Cytokines in atherosclerosis:key players in all stages of disease and promising therapeutic targets[J]. Cytokine Growth Factor Rev,2015,26(6):673-685.
[4]Edfeldt K,Agerberth B,Rottenberg ME,et al. Involvement of theantimicrobial peptide LL-37 in human a therosclerosis[J]. Arterioscler Thromb Vasc Biol,2006,26(7):1551-1557.
[5]D?ring Y,Drechsler M,Wantha S,et al. Lack of neutrophil-derived CRAMP reduces atherosclerosis in mice[J]. Circ Res,2012,110(8):1052-1056.
[6]Carbone F,Mach F,Montecucco F. Update on the role of neutrophils in atherosclerotic plaque vulnerability[J]. Curr Drug Targets,2015,16(4):321-333.
[7]Pende A,Artom N,Bertolotto M,et al. Role of neutrophils in atherogenesis:an update[J]. Eur J Clin Invest,2016,46(3):252-263.
[8]Pugliese G,Iacobini C,Blasetti Fantauzzi C,et al. The dark and bright side of atherosclerotic calcification[J]. Atherosclerosis,2015,238(2):220-230.
[9]Chistiakov DA,Orekhov AN,Bobryshev YV. Contribution of neovascularization and intraplaque haemorrhage to atherosclerotic plaque progression and instability[J]. Acta Physiol (Oxf),2015,213(3):539-553.
[10]Ionita MG,van den Borne P,Catanzariti LM,et al. High neutrophil numbers in human carotidatherosclerotic plaques are associated with characteristics of rupture-prone lesions[J]. Arterioscler Thromb Vasc Biol,2010,30(9):1842-1848.
[11]Driscoll WS,Vaisar T,Tang JJ,et al. Macrophage ADAM17 deficiency augments CD36-dependent apoptotic cell uptake and the linked anti-inflammatory phenotype[J]. CircRes,2013,113(1):52-61.
[12]Hartwig H,Silvestre Roig C,Daemen M,et al. Neutrophils in atherosclerosis. A brief overview[J]. Hamostaseologie,2015,35(2):121-127.
[13]Silvestre-Roig C,Braster Q,Wichapong K,et al. Externalized histone H4 orchestrates chronic inflammation by inducing lytic cell death[J]. Nature,2019,569(7755):236-240.
[14]D?ring Y,Manthey HD,Drechsler M,et al. Auto-antigenic protein-DNA complexes stimulate plasmacytoid dendritic cells to promote atherosclerosis[J]. Circulation,2012,125(13):1673-1683.
[15]Goossens P,Gijbels MJJ,Zernecke A,et al. Myeloid type I interferon signaling promotesatherosclerosis by stimulating macrophage recruitment to lesions[J]. Cell Metab,2010,12(2):142-153.
[16]Knight JS,Luo W,O’Dell AA,et al. Peptidylarginine deiminase inhibition reduces vascular damage and modulates innate immune responses in murine models of atherosderosis[J]. Cire Res,2014,114(6):947-956.
[17]Kojima Y,Weissman IL,Leeper NJ. The role of efferocytosis in atherosclerosis[J]. Circulation,2017,135(5):476-489.
[18]Jia HB,Abtahian F,Aguirre AD,et al. In vivo diagnosis of plaque erosion and calcifiednodule in patients with acute coronary syndrome by intravascular optical coherence tomography[J]. J Am Coll Cardiol,2013,62(19):1748-1758.
[19]Quillard T,Araújo HA,Franck G,et al. Editor’s choice:TLR2 and neutrophils potentiate endothelial stress,apoptosis and detachment:implications for superficial erosion[J]. Eur HeartJ,2015,36(22):1394-1404.
[20]Mangold A,Alias S,Scherz T,et al. Coronary neutrophil extracellular trap burden and dnase activity in ST-elevation acute coronary syndrome are predictors of ST-segment resolution and infarct size[J]. Circ Res,2015,116(7):1182-1192.
[21]Ge L,Zhou X,Ji WJ,et al. Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow:therapeutic potential of DNase-based reperfusion strategy[J]. Am J Physiol Heart Circ Physiol,2015,308(5):H500-H509.
[22]Riegger J,Byrne RA,Joner M,et al. Histopathological evaluation of thrombus in patients presenting with stent thrombosis. A multicenter European study:a report of the prevention of late stent thrombosis by an interdisciplinary global European effort consortium[J]. Eur Heart J,2016,37(19):1538-1549.
[23]Fuchs TA,Brill A,Duerschmied D,et al. Extracellular DNA traps promote thrombosis[J]. Proc Natl Acad Sci U S A,2010,107(36):15880-15885.
[24]Wang YB,Liu XY,Xia PP,et al. The regulatory role of microRNAs on phagocytes:a potential therapeutic target for chronic diseases[J]. Front Immunol,2022,13:901166-901185.
[25]Warnatsch A,Ioannou M,Wang Q,et al. Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis[J]. Science,2015,349(6245):316-320.
[26]Pertiwi KR,van der Wal AC,Pabittei DR,et al. Neutrophil extracellular traps participate in alldifferent types of thrombotic and haemorrhagic complications of coronary atherosclerosis[J]. Thromb Haemost,2018,118(6):1078-1087.
[27]Dai JN,Xing L,Jia HB,et al. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction:a clinical, angiographical, and intravascular optical coherence tomography study[J]. Eur Heart J,2018,39(22):2077-2085.
[28]Wang QZ,Zhao H,Qi N,et al. Generation and stability of size-adjustable bulk nanobubbles based on periodic pressure change[J]. Sci Rep,2019,9(1):1118-1126.
[29]Langseth MS,Opstad TB,Bratseth V,et al. Markers of neutrophil extracellular traps are associated with adverse clinical outcome in stable coronary artery disease[J]. Eur J Prev Cardiol,2018,25(7):762-769.
[30]Liu CQ,Desikan R,Ying ZK,et al. Effects of a novel pharmacologic inhibitor of myeloperoxidase in a mouse atherosclerosis model[J]. PLoS One,2012,7(12):e50767-e50777.
[31]Ali M,Pulli B,Courties G,et al. Myeloperoxidase inhibition improves ventricular function and remodeling after experimental myocardial infarction[J]. JACC Basic Transl Sci,2016,1(7):633-643.
[32]Fukuta T,Okada H,Takemura G,et al. Neutrophil elastase inhibition ameliorates endotoxin-induced myocardial injury accompanying degradation of cardiac capillary glycocalyx[J]. Shock,2020,54(3):386-393.
[33]Bidouard JP,Duval N,Kapui Z,et al. SSR69071,an elastase inhibitor, reduces myocardial infarct size following ischemia-reperfusion injury[J]. Eur J Pharmacol,2003,461(1):49-52.
[34]Schumski A,Ortega-Gómez A,Wichapong K,et al. Endotoxinemia Accelerates Atherosclerosis through Electrostatic Charge-Mediated Monocyte Adhesion[J]. Circulation,2021,143(3):254-266.
[35]Connolly SJ,Eikelboom JW,Bosch J,et al. Rivaroxaban with or without aspirin in patients with stable coronary artery disease:an international,randomised,double-blind,placebo-controlledtrial[J].Lancet,2018,391(10117):205-218.
[36]Healy LD,Puy C,Itakura A,et al. Colocalization of neutrophils,extracellular DNA and coagulation factors during NETosis:development and utility of an immunofluorescence-basemicroscopy platform[J]. J Immunol Methods,2016,435:77-84.
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