Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (6): 660-663.doi: 10.7518/gjkq.2017.06.007
• Periodontitis • Previous Articles Next Articles
Tang Qiuling, Li Gege, Pan Jiahui, Hou Yubo, Meng Yang, Yu Weixian.
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| [1] Ghonime MG, Shamaa OR, Eldomany RA, et al. Tyro-sine phosphatase inhibition induces an ASC-depen-dent pyroptosis[J]. Biochem Biophys Res Commun, 2012, 425(2):384-389. [2] Bostanci N, Emingil G, Saygan B, et al. Expression and regulation of the NALP3 inflammasome complex in periodontal diseases[J]. Clin Exp Immunol, 2009, 157(3):415-422. [3] Blander JM. A long-awaited merger of the pathways mediating host defence and programmed cell death [J]. Nat Rev Immunol, 2014, 14(9):601-618. [4] Galluzzi L, Vitale I, Abrams JM, et al. Molecular definitions of cell death subroutines: recommenda-tions of the Nomenclature Committee on Cell Death 2012[J]. Cell Death Differ, 2012, 19(1):107-120. [5] Shi JJ, Zhao YE, Wang K, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015, 526(7575):660-665. [6] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44. [7] Broz P. Immunology: caspase target drives pyroptosis [J]. Nature, 2015, 526(7575):642-643. [8] Lim Y, Kumar S. A single cut to pyroptosis[J]. Onco-target, 2015, 6(35):36926-36927. [9] He WT, Wan H, Hu L, et al. Gasdermin D is an exe-cutor of pyroptosis and required for interleukin-1β secretion[J]. Cell Res, 2015, 25(12):1285-1298. [10] Genco RJ, Van Dyke TE. Prevention: reducing the risk of CVD in patients with periodontitis[J]. Nat Rev Cardiol, 2010, 7(9):479-480. [11] Takahashi Y, Davey M, Yumoto H, et al. Fimbria-dependent activation of pro-inflammatory molecules in Porphyromonas gingivalis infected human aortic endothelial cells[J]. Cell Microbiol, 2006, 8(5):738- 757. [12] Kataoka H, Kono H, Patel Z, et al. Evaluation of the contribution of multiple DAMPs and DAMP recep-tors in cell death-induced sterile inflammatory res-ponses[J]. PLoS One, 2014, 9(8):e104741. [13] Ito Y, Bhawal UK, Sasahira T, et al. Involvement of HMGB1 and RAGE in IL-1β-induced gingival infla-mmation[J]. Arch Oral Biol, 2012, 57(1):73-80. [14] Li G, Liang X, Lotze MT. HMGB1: the central cyto-kine for all lymphoid cells[J]. Front Immunol, 2013, 4(4):68. [15] Andersson U, Tracey KJ. HMGB1 is a therapeutic target for sterile inflammation and infection[J]. Annu Rev Immunol, 2011, 29:139-162. [16] Di Benedetto A, Gigante I, Colucci S, et al. Perio-dontal disease: linking the primary inflammation to bone loss[J]. Clin Dev Immunol, 2013, 2013:503754. [17] Chakraborty R, Bhatt KH, Sodhi A. High mobility group box 1 protein synergizes with lipopolysacc-haride and peptidoglycan for nitric oxide production in mouse peritoneal macrophages in vitro [J]. Mol Immunol, 2013, 54(1):48-57. [18] Man SM, Kanneganti TD. Gasdermin D: the long-awaited executioner of pyroptosis[J]. Cell Res, 2015, 25(11):1183-1184. [19] Schroder K, Tschopp J. The inflammasones[J]. Cell, 2010, 140(6):821-832. [20] Shi JJ, Zhao YE, Wang YP, et al. Inflammatory cas-pases are innate immune receptors for intracellular LPS[J]. Nature, 2014, 514(7521):187. [21] 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. [22] Benedyk M, Mydel PM, Delaleu N, et al. Gingipains: critical factors in the development of aspiration pne-umonia caused by Porphyromonas gingivalis [J]. J Innate Immun, 2016, 8(2):185-198. [23] Lausson S, Cressent M. Signal transduction pathways mediating the effect of adrenomedullin on osteoblast survival[J]. J Cell Biochem, 2011, 112(12):3807- 3815. [24] 陈玉婷, 宋祥晨, 张福萍, 等. 促凋亡蛋白Bim、Bax和Bak在牙龈蛋白酶诱导成骨细胞凋亡中的表达[J]. 中华口腔医学杂志, 2013, 48(5):272-277. Chen YT, Song XC, Zhang FP, et al. Expression of Bim, Bax and Bak in the process of gingipain-induced osteoblast apoptosis[J]. Chin J Stomatol, 2013, 48 (5):272-277. [25] Huang MT, Taxman DJ, Holley-Guthrie EA, et al. Critical role of apoptotic speck protein containing a caspase recruitment domain(ASC) and NLRP3 in causing necrosis and ASC speck formation induced by Porphyromonas gingivalis in human cells[J]. J Immunol, 2009, 182(4):2395-2404. [26] Kolev M, Le Friec G, Kemper C. Complement—tap-ping into new sites and effector systems[J]. Nat Rev Immunol, 2014, 14(12):811-820. [27] Maekawa T, Krauss JL, Abe T, et al. Porphyromonas gingivalis manipulates complement and TLR signa-ling to uncouple bacterial clearance from inflamma-tion and promote dysbiosis[J]. Cell Host Microbe, 2014, 15(6):768-778. |