[1] Chen WW, Gao RL, Liu LSh, et al. Summary of China cardiovascular disease report 2016[J]. Chinese Circulation Journal, 2017, 32 (6): 521-530. (in Chinese)
陈伟伟, 高润霖, 刘力生, 等. 《中国心血管病报告2016》概要[J]. 中国循环杂志, 2017, 32(6): 521-530.
[2] Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J]. Nature, 2010, 464(7293): 1357-1361.
[3] Byon CH, Han T, Wu J, et al. Txnip ablation reduces vascular smooth muscle cell inflammation and ameliorates atherosclerosis in apolipoprotein E knockout mice[J]. Atherosclerosis, 2015, 241(2):313-321.
[4] Gage J, Hasu M, Thabet M, et al. Caspase-1 deficiency decreases atherosclerosis in apolipoprotein E-null mice[J]. Can J Cardiol, 2012, 28(2): 222-229.
[5] Shen J, Yin Y, Mai J, et al. Caspase-1 recognizes extended cleavage sites in its natural substrates[J]. Atherosclerosis, 2010, 210(2): 422-429.
[6] Ulleryd MA, Prahl U, Brsbo J, et al. The association between autonomic dysfunction, inflammation and atherosclerosis in men under investigation for carotid plaques[J]. PLoS One, 2017, 12(4): e0174974.
[7] King SM, Mcnamee RA, Houng AK, et al. Platelet dense-granule secretion plays a critical role in thrombosis and subsequent vascular remodeling in atherosclerotic mice[J]. Circulation, 2009, 120(9): 785-791.
[8] Ballinger SW, Patterson C, Knight-Lozano CA, et al. Mitochondrial integrity and function in atherogenesis[J]. Circulation, 2002, 106(5): 544-549.
[9] Yin Y, Li X, Sha X, et al. Early hyperlipidemia promotes endothelial activation via a caspase-1-sirtuin 1 pathway[J]. Arterioscler Thromb Vasc Biol, 2015, 35(4): 804-816.
[10]Xi H, Zhang Y, Xu Y, et al. Caspase-1 inflammasome activation mediates homocysteine-iduced pyrop-apoptosis in endothelial cells[J]. Circ Res, 2016, 118(10): 1525-1539.
[11]Chistiakov DA, Grechko AV, Myasoedova VA, et al. The role of monocytosis and neutrophilia in atherosclerosis[J]. J Cell Mol Med, 2018, 22(3): 1366-1382.
[12]Laufer EM, Winkens MH, Narula J, et al. Molecular imaging of macrophage cell death for the assessment of plaque vulnerability[J]. Arterioscler Thromb Vasc Biol, 2009, 29(7): 1031-1038.
[13]Chen C, Khismatullin DB. Oxidized low-density lipoprotein contributes to atherogenesis via co-activation of macrophages and mast cells[J]. PLoS One, 2015, 10(3):e0123088.
[14]Fredman G, Hellmann J, Proto JD, et al. An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques[J]. Nat Commun, 2016, 7:12859.
[15]Forte L, Cimmino G, Loffredo F, et al. C-reactive protein is released in the coronary circulation and causes endothelial dysfunction in patients with acute coronary syndromes[J]. Int J Cardiol, 2011, 152(1): 7-12.
[16]Ridker PM. From C-reactive protein to interleukin-6 to interleukin-1: moving upstream to identify novel targets for atheroprotection[J]. Circ Res, 2016, 118(1): 145-156.
[17]Han Y, Qiu H, Pei X, et al. Low-dose sinapic acid abates the pyroptosis of macrophages by downregulation of lncRNA-MALAT1 in rats with diabetic atherosclerosis[J]. J Cardiovasc Pharmacol, 2018, 71(2): 104-112.
[18]Yang H, Xiao L, Yuan Y, et al. Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells[J]. Biochem Pharmacol, 2014, 92(4): 599-606.
[19]Miao EA, Leaf IA, Treuting PM, et al. Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria[J]. Nat Immunol, 2010, 11(12): 1136-1142.
[20]Haldar S, Dru C, Choudhury D, et al. Inflammation and pyroptosis mediate muscle expansion in an interleukin-1beta (IL-1beta)-dependent manner[J]. J Biol Chem, 2015, 290(10): 6574-6583.
[21]Yang D, He Y, Mu?oz-Planillo R, et al. Caspase-11 requires the pannexin-1 channel and the purinergic P2X7 pore to mediate pyroptosis and endotoxic shock[J]. Immunity, 2015, 43(5): 923-932.
[22]Kayagaki N, Stowe IB, Lee BL, et al. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling[J]. Nature, 2015, 526(7575): 666-671.
[23]Zhang Y, Mu Q, Zhou Z, et al. Protective effect of irisin on atherosclerosis via suppressing oxidized low density lipoprotein induced vascular inflammation and endothelial dysfunction[J]. PLoS One, 2016, 11(6): e0158038.
[24]Yan H, Li Y, Peng X, et al. Resistance of mitochondrial DNA-depleted cells against oxidized low-density lipoprotein-induced macrophage pyroptosis[J]. Mol Med Rep, 2016, 13(5): 4393-4399.
[25]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[J]. Nat Immunol, 2013, 14(8): 812-820.
[26]Jiang Y, Wang M, Huang K, et al. Oxidized low-density lipoprotein induces secretion of interleukin-1beta by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation[J]. Biochem Biophys Res Commun, 2012, 425(2):121-126.
[27]Afrasyab A, Qu P, Zhao Y, et al. Correlation of NLRP3 with severity and prognosis of coronary atherosclerosis in acute coronary syndrome patients[J]. Heart Vessels, 2016, 31(8): 1218-1229.
[28] Rajam?ki K, Lappalainen J, O?rni K, et al. Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation[J]. PLoS One, 2010, 5(7): e11765.
[29]Lai D, Tang J, Chen L, et al. Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis[J]. Cell Death Dis, 2018, 9(3): 369-380.
[30]Liu W, Chen Y, Meng J, et al. Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo[J]. J Neuroinflammation, 2018, 15(1): 48-63.
[31]Clarke MC, Talib S, Figg NL, et al. Vascular smooth muscle cell apoptosis induces interleukin-1-directed inflammation: effects of hyperlipidemia-mediated inhibition of phagocytosis[J]. Circ Res, 2010, 106(2): 363-372.
[32]Wu X, Zhang H, Qi W, et al. Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis[J]. Cell Death Dis, 2018, 9(2): 171-182.
[33]Compan Ⅴ, Barojamazo A, Lópezcastejón G, et al. Apoptosis-associated speck-like protein containing a CARD forms specks but does not activate caspase-1 in the absence of NLRP3 during macrophage swelling[J]. J Immunol, 2015, 194(3): 1261-1273.
[34]Suzuki T, Franchi L, Toma C, et al. Differential regulation of caspase-1 activation, pyroptosis, and autophagy via Ipaf and ASC in Shigella-infected macrophages[J]. PLoS Pathog, 2007, 3(8): e111.
[35]Wang R, Wang Y, Mu N, et al. Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in apoE-deficient mice[J]. Lab Invest, 2017, 97(8): 922-934.
[36]Triantafilou K, Hughes TR, Triantafilou M, et al. The complement membrane attack complex triggers intracellular Ca2+fluxes leading to NLRP3 inflammasome activation[J]. J Cell Sci, 2013, 126(13): 2903-2913.
[37]Chen H, Lu Y, Cao Z, et al. Cadmium induces NLRP3 inflammasome-dependent pyroptosis in vascular endothelial cells[J]. Toxicol Lett, 2016, 246: 7-16.
[38]Hu Q, Zhang T, Yi L, et al. Dihydromyricetin inhibits NLRP3 inflammasomedependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells[J]. Biofactors, 2018, 44(2):123-136.
[39]Liu T, Zeng Y, Tang K, et al. Dihydromyricetin ameliorates atherosclerosis in LDL receptor deficient mice[J]. Atherosclerosis, 2017, 262: 39-50.
[40]Kinoshita T, Imamura R, Kushiyama H, et al. NLRP3 mediates NF-kappaB activation and cytokine induction in microbially induced and sterile inflammation[J]. PLoS One, 2015, 10(3): e0119179.
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