[1] Wang XD, Zhang JN, Gan YH, et al. Current understanding of pathogenesis and treatment of TMJ osteoarthritis [J]. J Dent Res, 2015, 94(5): 666-673. [2] Feng Y, Fang W, Li C, et al. The expression of high-mobility group box protein-1 in temporomandibular joint osteoarthritis with disc perforation [J]. J Oral Pathol Med, 2016, 45(2): 148-152. [3] Goodwin GH, Johns EW. Isolation and characterisation of two calf-thymus chromatin non-histone proteins with high contents of acidic and basic amino acids [J]. Eur J Biochem, 1973, 40(1): 215-219. [4] Wang H, Bloom O, Zhang M, et al. HMG-1 as a late mediator of endotoxin lethality in mice [J]. Science, 1999, 285(5425): 248-251. [5] Bonaldi T, Talamo F, Scaffidi P, et al. Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion [J]. EMBO J, 2003, 22(20): 5551-5560. [6] Andersson U, Yang H,Harris H. High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells [J]. Semin Immunol, 2018, 38: 40-48. [7] Tang Y, Zhao X, Antoine D, et al. Regulation of posttranslational modifications of HMGB1 during immune responses [J]. Antioxid Redox Signal, 2016, 24(12): 620-634. [8] Harris HE, Andersson U, Pisetsky DS.HMGB1: a multifunctional alarmin driving autoimmune and inflammatory disease [J]. Nat Rev Rheumatol, 2012, 8(4): 195-202. [9] Scaffidi P, Misteli T, Bianchi ME. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation [J]. Nature, 2002, 418(6894): 191-195. [10] Ito I, Fukazawa J, Yoshida M. Post-translational methylation of high mobility group box 1 (HMGB1) causes its cytoplasmic localization in neutrophils [J]. J Biol Chem, 2007, 282(22): 16336-16344. [11] Gardella S, Andrei C, Ferrera D, et al. The nuclear protein HMGB1 is secreted by monocytes via a non-classical, vesicle-mediated secretory pathway [J]. EMBO Rep, 2002, 3(10): 995-1001. [12] Pellegrini L, Foglio E, Pontemezzo E, et al. HMGB1 and repair: focus on the heart [J]. Pharmacol Ther, 2019, 196: 160-182. [13] Andersson U, Yang H,Harris H. Extracellular HMGB1 as a therapeutic target in inflammatory diseases [J]. Expert Opin Ther Targets, 2018, 22(3): 263-277. [14] Bell CW, Jiang W, Reich CF, et al. The extracellular release of HMGB1 during apoptotic cell death [J]. Am J Physiol Cell Physiol, 2006, 291(6): C1318-C1325. [15] Kazama H, Ricci JE, Herndon JM, et al. Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein [J]. Immunity, 2008, 29(1): 21-32. [16] Deng M, Scott MJ, Fan J, et al. Location is the key to function: HMGB1 in sepsis and trauma-induced inflammation [J]. J Leukoc Biol, 2019, 106(1): 161-169. [17] Stark K, Philippi V, Stockhausen S, et al. Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice [J]. Blood, 2016, 128(20): 2435-2449. [18] Bianchi ME. HMGB1 loves company [J]. J Leukoc Biol, 2009, 86(3): 573-576. [19] Thorburn J, Frankel AE, Thorburn A. Regulation of HMGB1 release by autophagy [J]. Autophagy, 2009, 5(2): 247-249. [20] Venereau E, Casalgrandi M, Schiraldi M, et al.Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release [J]. J Exp Med, 2012, 209(9): 1519-1528. [21] Yang H, Wang H,Andersson U. Targeting Inflammation Driven by HMGB1 [J]. Front Immunol, 2020, 11: 484. [22] Paudel YN, Angelopoulou E, Piperi C, et al. Enlightening the role of high mobility group box 1 (HMGB1) in inflammation: Updates on receptor signalling [J]. Eur J Pharmacol, 2019, 858: 172487. [23] Riuzzi F, Sorci G, Sagheddu R, et al. RAGE in the pathophysiology of skeletal muscle [J]. J Cachexia Sarcopenia Muscle, 2018, 9(7): 1213-1234. [24] Alam SI, Rehman SU, Kim MO. Nicotinamide improves functional recovery via regulation of the RAGE/JNK/NF-kappaB signaling pathway after brain injury [J]. J Clin Med, 2019, 8(2). [25] Tripathi A, Shrinet K,Kumar A. HMGB1 protein as a novel target for cancer [J]. Toxicol Rep, 2019, 6: 253-261. [26] Beutler B. TLR4 as the mammalian endotoxin sensor [J]. Curr Top Microbiol Immunol, 2002, 270: 109-120. [27] Visintin A, Iliev DB, Monks BG, et al. MD-2 [J]. Immunobiology, 2006, 211(6-8): 437-447. [28] Park BS, Song DH, Kim HM, et al.The structural basis of lipopolysaccharide recognition by the TLR4-MD-2 complex [J]. Nature, 2009, 458(7242): 1191-1195. [29] Yang H, Wang H, Ju Z, et al. MD-2 is required for disulfide HMGB1-dependent TLR4 signaling [J]. J Exp Med, 2015, 212(1): 5-14. [30] Meng L, Li L, Lu S, et al. The protective effect of dexmedetomidine on LPS-induced acute lung injury through the HMGB1-mediated TLR4/NF-kappaB and PI3K/Akt/mTOR pathways [J]. Mol Immunol, 2018, 94: 7-17. [31] Fu Y, Lei J, Zhuang Y, et al. Overexpression of HMGB1 A-box reduced IL-1beta-induced MMP expression and the production of inflammatory mediators in human chondrocytes [J]. Exp Cell Res, 2016, 349(1): 184-190. [32] Biscetti F, Flex A, Pecorini G, et al. The role of high-mobility group box protein 1 in collagen antibody-induced arthritis is dependent on vascular endothelial growth factor [J]. Clin Exp Immunol, 2016, 184(1): 62-72. [33] Sun XH, Liu Y, Han Y, et al. Expression and significance of high-mobility group protein B1 (HMGB1) and the receptor for advanced glycation end-product (RAGE) in knee osteoarthritis [J]. Med Sci Monit, 2016, 22: 2105-2112. [34] Amin AR, Islam AB. Genomic analysis and differential expression of HMG and S100A family in human arthritis: upregulated expression of chemokines, IL-8 and nitric oxide by HMGB1 [J]. DNA Cell Biol, 2014, 33(8): 550-565. [35] Ke X, Jin G, Yang Y, et al. Synovial fluid HMGB-1 levels are associated with osteoarthritis severity [J]. Clin Lab, 2015, 61(7): 809-818. [36] Garcia-Arnandis I, Guillen MI, Castejon MA, et al. Haem oxygenase-1 down-regulates high mobility group box 1 and matrix metalloproteinases in osteoarthritic synoviocytes [J]. Rheumatology (Oxford), 2010, 49(5): 854-861. [37] Terada C, Yoshida A, Nasu Y, et al. Gene expression and localization of high-mobility group box chromosomal protein-1 (HMGB-1)in human osteoarthritic cartilage [J]. Acta Med Okayama, 2011, 65(6): 369-377. [38] Loeser RF, Yammani RR, Carlson CS, et al. Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis [J]. Arthritis Rheum, 2005, 52(8): 2376-2385. [39] Garcia-Arnandis I, Guillen MI, Gomar F, et al. High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1beta in osteoarthritic synoviocytes [J]. Arthritis Res Ther, 2010, 12(4): R165. [40] Wahamaa H, Schierbeck H, Hreggvidsdottir HS, et al. High mobility group box protein 1 in complex with lipopolysaccharide or IL-1 promotes an increased inflammatory phenotype in synovial fibroblasts [J]. Arthritis Res Ther, 2011, 13(4): R136. [41] Li C, Cai H, Meng Q, et al. IL-1beta mediating high mobility group box protein-1 expression in condylar chondrocyte during temporomandibular joint inflammation [J]. J Oral Pathol Med, 2016, 45(7): 539-545. [42] Feng Y, Ke J, Cao P, et al. HMGB1-induced angiogenesis in perforated disc cells of human temporomandibular joint [J]. J Cell Mol Med, 2018, 22(2): 1283-1291. [43] Khan MI, Rath S, Adhami VM, et al.Hypoxia driven glycation: Mechanisms and therapeutic opportunities [J]. Semin Cancer Biol, 2018, 49: 75-82. |