［2］Singh JA, Gaffo A. Gout epidemiology and comorbidities［J］. Semin Arthritis Rheum, 2020, 50(3S): S11-S16.

［3］赵敏, 陈婷, 黄振光, 等. 1990—2019年中国痛风疾病负担研究［J］. 现代预防医学, 2021, 48(21): 3974-3978.

［4］Keysser G. Gout arthritis: pathogenesis, diagnostics and treatment［J］. Dtsch Med Wochenschr, 2020, 145(14): 991-1005.

［5］VargasSantos AB, Neogi T, da Rocha CastelarPinheiro G, et al. Causespecific mortality in gout: novel findings of elevated risk of noncardiovascularrelated deaths［J］. Arthritis Rheumatol, 2019, 71(11): 1935-1942.

［6］Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria［J］. Science, 2004, 303(5663): 1532-1535.

［7］Pieterse E, Jeremic I, Czegley C, et al. Bloodborne phagocytes internalize urate microaggregates and prevent intravascular NETosis by urate crystals［J］. Sci Rep, 2016, 6: 38229.

［8］Liu L, Wang D, Liu M, et al. The development from hyperuricemia to gout: key mechanisms and natural products for treatment［J］. AHM, 2022, 2(1): 25-32.

［9］Yan F, Zhang H, Yuan X, et al. Comparison of the different monosodium urate crystals in the preparation process and proinflammation［J］. Adv Rheumatol, 2023, 63(1): 39.

［10］Chen C, Wang J, Liang Z, et al. Monosodium urate crystals with controlled shape and aspect ratio for elucidating the pathological progress of acute gout［J］. Biomater Adv, 2022, 139: 213005.

［11］Towiwat P, Chhana A, Dalbeth N. The anatomical pathology of gout: a systematic literature review［J］. BMC Musculoskelet Disord, 2019, 20(1): 140.

［12］Dalbeth N, Stamp L. Hyperuricaemia and gout: time for a new staging system?［J］. Ann Rheum Dis, 2014, 73(9): 1598-1600.

［13］Schett G, Schauer C, Hoffmann M, et al. Why does the gout attack stop? A roadmap for the immune pathogenesis of gout［J］. RMD Open, 2015, 1(Suppl 1): e000046.

［14］Takei H, Araki A, Watanabe H, et al. Rapid killing of human neutrophils by the potent activator phorbol 12myristate 13acetate (PMA) accompanied by changes different from typical apoptosis or necrosis［J］. J Leukoc Biol, 1996, 59(2): 229-240.

［15］Brinkmann V, Zychlinsky A. Neutrophil extracellular traps: Is immunity the second function of chromatin?［J］. J Cell Biol, 2012, 198(5): 773-783.

［16］Branzk N, Lubojemska A, Hardison SE, et al. Neutrophils sense microbe size and selectively release neutrophil extracellular traps in response to large pathogens［J］. Nat Immunol, 2014, 15(11): 1017-1025.

［17］Steinberg BE, Grinstein S. Unconventional roles of the NADPH oxidase: signaling, ion homeostasis, and cell death［J］. Sci STKE, 2007, 2007(379): pe11.

［18］Hamam HJ, Palaniyar N. Posttranslational modifications in NETosis and NETsmediated diseases［J］. Biomolecules, 2019, 9(8): 369.

［19］Yipp BG, Kubes P. NETosis: how vital is it?［J］. Blood, 2013, 122(16): 2784-2794.

［20］Klopf J, Brostjan C, Eilenberg W, et al. Neutrophil extracellular traps and their implications in cardiovascular and inflammatory disease［J］. Int J Mol Sci, 2021, 22(2): 559.

［21］Farrera C, Fadeel B. Macrophage clearance of neutrophil extracellular traps is a silent process［J］. J Immunol, 2013, 191(5): 2647-2656.

［22］Yaykasli KO, Schauer C, Munoz LE, et al. Neutrophil extracellular trapdriven occlusive diseases［J］. Cells, 2021, 10(9): 2208.

［23］Daniel C, Leppkes M, Munoz LE, et al. Extracellular DNA traps in inflammation, injury and healing［J］. Nat Rev Nephrol, 2019, 15(9): 559-575.

［24］Muoz LE, Bilyy R, Biermann MH, et al. Nanoparticles sizedependently initiate selflimiting NETosisdriven inflammation［J］. Proc Natl Acad Sci U S A, 2016, 113(40): E5856-E5865.

［25］Schauer C, Janko C, Munoz LE, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines［J］. Nat Med, 2014, 20(5): 511-517.

［26］Chatfield SM, Grebe K, Whitehead LW, et al. Monosodium urate crystals generate nucleaseresistant neutrophil extracellular traps via a distinct molecular pathway［J］. J Immunol, 2018, 200(5): 1802-1816.

［27］Chen X, Li W, Ren J, et al. Translocation of mixed lineage kinase domainlike protein to plasma membrane leads to necrotic cell death［J］. Cell Res, 2014, 24(1): 105-121.

［28］Desai J, Kumar SV, Mulay SR, et al. PMA and crystalinduced neutrophil extracellular trap formation involves RIPK1RIPK3MLKL signaling［J］. Eur J Immunol, 2016, 46(1): 223-229.

［29］Remijsen Q, Vanden Berghe T, Wirawan E, et al. Neutrophil extracellular trap cell death requires both autophagy and superoxide generation［J］. Cell Res, 2011, 21(2): 290-304.

［30］Mitroulis I, Kambas K, Chrysanthopoulou A, et al. Neutrophil extracellular trap formation is associated with IL1β and autophagyrelated signaling in gout［J］. PLoS One, 2011, 6(12): e29318.

［31］Tan H, Li Z, Zhang S, et al. Novel perception of neutrophil extracellular traps in gouty inflammation［J］. Int Immunopharmacol, 2023, 115: 109642.

［32］Liu C, Zhou M, Jiang W, et al. GPR105targeted therapy promotes gout resolution as a switch between NETosis and apoptosis of neutrophils［J］. Front Immunol, 2022, 13: 870183.

［33］Sil P, Hayes CP, Reaves BJ, et al. P2Y6 receptor antagonist MRS2578 inhibits neutrophil activation and aggregated neutrophil extracellular trap formation induced by goutassociated monosodium urate crystals［J］. J Immunol, 2017, 198(1): 428-442.

［34］Schoen J, Euler M, Schauer C, et al. Neutrophils′ extracellular trap mechanisms: From physiology to pathology［J］. Int J Mol Sci, 2022, 23(21): 12855.

［35］Taylor WJ, Fransen J, Jansen TL, et al. Study for updated gout classification criteria: identification of features to classify gout［J］. Arthritis Care Res (Hoboken), 2015, 67(9): 1304-1315.

［36］Chen YH, Hsieh SC, Chen WY, et al. Spontaneous resolution of acute gouty arthritis is associated with rapid induction of the antiinflammatory factors TGFβ1, IL10 and soluble TNF receptors and the intracellular cytokine negative regulators CIS and SOCS3［J］. Ann Rheum Dis, 2011, 70(9): 1655-1663.

［37］So AK, Martinon F. Inflammation in gout: mechanisms and therapeutic targets［J］. Nat Rev Rheumatol, 2017, 13(11): 639-647.

［38］Schorn C, Frey B, Lauber K, et al. Sodium overload and water influx activate the NALP3 inflammasome［J］. J Biol Chem, 2011, 286(1): 35-41.

［39］Kelley N, Jeltema D, Duan Y, et al. The NLRP3 inflammasome: An overview of mechanisms of activation and regulation［J］. Int J Mol Sci, 2019, 20(13): 3328.

［40］Chen CJ, Shi Y, Hearn A, et al. MyD88dependent IL1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals［J］. J Clin Invest, 2006, 116(8): 2262-2271.

［41］Dalbeth N, Pool B, Gamble GD, et al. Cellular characterization of the gouty tophus: a quantitative analysis［J］. Arthritis Rheum, 2010, 62(5): 1549-1556.

［42］GarciaGonzalez E, Gamberucci A, Lucherini OM, et al. Neutrophil extracellular traps release in gout and pseudogout depends on the number of crystals regardless of leukocyte count［J］. Rheumatology (Oxford), 2021, 60(10): 4920-4928.

［43］Desai J, Steiger S, Anders HJ. Molecular pathophysiology of gout［J］. Trends Mol Med, 2017, 23(8): 756-768.

［44］Dalbeth N, Aati O, Kalluru R, et al. Relationship between structural joint damage and urate deposition in gout: a plain radiography and dualenergy CT study［J］. Ann Rheum Dis, 2015, 74(6): 1030-1036.

［45］Schlesinger N, Thiele RG. The pathogenesis of bone erosions in gouty arthritis［J］. Ann Rheum Dis, 2010, 69(11): 1907-1912.

［46］Jia E, Li Z, Geng H, et al. Neutrophil extracellular traps induce the bone erosion of gout［J］. BMC Musculoskelet Disord, 2022, 23(1): 1128.

［47］周梦, 陈志涵, 郑炜平, 等. 高尿酸血症促进大鼠海马组织中β淀粉样蛋白沉积的机制研究［J］. 江苏大学学报(医学版), 2023, 33(2): 141-145.

［48］孙宇焱. 高尿酸血症在2型糖尿病血管并发症中的作用［J］. 江苏大学学报(医学版), 2007, 17(2): 178-179.

［49］Bonaventura A, Vecchié A, Abbate A, et al. Neutrophil extracellular traps and cardiovascular diseases: an update［J］. Cells, 2020, 9(1): 231.

［50］Mutua V, Gershwin LJ. A review of neutrophil extracellular traps (NETs) in disease: potential antiNETs therapeutics［J］. Clin Rev Allergy Immunol, 2021, 61(2): 194-211.

［51］Liu L, Shan L, Wang H, et al. Neutrophil extracellular trapborne elastase prevents inflammatory relapse in intercritical gout［J］. Arthritis Rheumatol, 2023, 75(6): 1039-1047.

［52］Vedder D, Gerritsen M, Duvvuri B, et al. Neutrophil activation identifies patients with active polyarticular gout［J］. Arthritis Res Ther, 2020, 22(1): 148.

［53］Euler M, Hoffmann MH. The doubleedged role of neutrophil extracellular traps in inflammation［J］. Biochem Soc Trans, 2019, 47(6): 1921-1930.

［54］Ngo ATP, Gollomp K. Building a better NET: Neutrophil extracellular trap targeted therapeutics in the treatment of infectious and inflammatory disorders［J］. Res Pract Thromb Haemost, 2022, 6(7): e12808.

［55］Martin Monreal MT, Rebak AS, Massarenti L, et al. Applicability of smallmolecule inhibitors in the study of peptidyl arginine deiminase 2 (PAD2) and PAD4［J］. Front Immunol, 2021, 12: 716250.

［56］Schorn C, Janko C, Latzko M, et al. Monosodium urate crystals induce extracellular DNA traps in neutrophils, eosinophils, and basophils but not in mononuclear cells［J］. Front Immunol, 2012, 3: 277.