HMGB1 Regulates RANKL-Induced Osteoclastogenesis in a Manner Dependent on RAGE
Open accessAbstract
High-mobility group box 1 (HMGB1), a nonhistone nuclear protein, is released by macrophages into the extracellular milieu consequent to cellular activation. Extracellular HMGB1 has properties of a pro-inflammatory cytokine through its interaction with receptor for advanced glycation endproducts (RAGE) and/or toll-like receptors (TLR2 and TLR4). Although HMGB1 is highly expressed in macrophages and differentiating osteoclasts, its role in osteoclastogenesis remains largely unknown. In this report, we present evidence for a function of HMGB1 in this event. HMGB1 is released from macrophages in response to RANKL stimulation and is required for RANKL-induced osteoclastogenesis in vitro and in vivo. In addition, HMGB1, like other osteoclastogenic cytokines (e.g., TNFα), enhances RANKL-induced osteoclastogenesis in vivo and in vitro at subthreshold concentrations of RANKL, which alone would be insufficient. The role of HMGB1 in osteoclastogenesis is mediated, in large part, by its interaction with RAGE, an immunoglobin domain containing family receptor that plays an important role in osteoclast terminal differentiation and activation. HMGB1-RAGE signaling seems to be important in regulating actin cytoskeleton reorganization, thereby participating in RANKL-induced and integrin-dependent osteoclastogenesis. Taken together, these observations show a novel function of HMGB1 in osteoclastogenesis and provide a new link between inflammatory mechanisms and bone resorption.
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HMGB1 and M-CSF have been suggested to be produced by osteocytes that stimulate osteoclast recruitment during bone remodeling.
“High mobility group box protein 1 (HMGB1) [198–200] and M-CSF [201] have also been suggested to be produced by osteocytes that stimulate osteoclast recruitment during bone remodeling [72, 73].”
From Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015) · cites this paper as [200]
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“Recently, the high mobility group box 1 (HMGB1) nuclear transcription factor, which can be released by damaged cells, was shown to upregulate maturation of osteoclasts by binding to advanced glycation endproduct receptors (254).”
BackgroundRAGE Signaling in Skeletal Biology
Plotkin, L. I., Essex, A. L., & Davis, H. M. (2019) · Current Osteoporosis Reports · doi:10.1007/s11914-019-00499-w · Cited by 54 · see citing works
Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review
Martinis, M. D., Ginaldi, L., Sirufo, M. M., Pioggia, G., Calapai, G., Gangemi, S., & Mannucci, C. (2020) · Medicina · doi:10.3390/medicina56030138 · Cited by 53 · see citing works
“Evidence supporting the role of extracellular HMGB1, as an autocrine ligand of RAGE, in RANKL-induced osteoclastogenesis in vitro and in vivo have been proposed [63].”
BackgroundWang, X., Schröder, H. C., Feng, Q., Draenert, F. G., & Müller, W. E. G. (2013) · Marine Drugs · doi:10.3390/md11030718 · Cited by 49 · see citing works
“osteoprotegerin (OPG), a cytokine that is expressed in osteoblasts with a significant role in the maturation of osteoclasts as well as in the control of bone mineral density [41], and the receptor activator of the NF-κB ligand (RANKL), a mediator that binds to RANK which is a receptor that mediates maturation of osteo…”
BackgroundPieters, B. C. H., Cappariello, A., van den Bosch, M. H. J., van Lent, P. L. E. M., Teti, A. M., & van de Loo, F. A. J. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01901 · Cited by 48 · see citing works
“HMGB1-RAGE signaling was shown to be important in regulating actin cytoskeleton reorganization, thereby contributing to RANKL-induced and integrin-dependent osteoclastogenesis (81).”
BackgroundHigh Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies
Datta, S., Rahman, M. A., Koka, S., & Boini, K. M. (2024) · Cells · doi:10.3390/cells13231946 · Cited by 48 · see citing works
Dual effect of inorganic polymeric phosphate/polyphosphate on osteoblasts and osteoclasts in vitro
Wang, X., Schröder, H. C., Diehl‐Seifert, B., Kropf, K., Schloßmacher, U., Wiens, M., & Müller, W. E. G. (2012) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.1465 · Cited by 48 · see citing works
“RANKL results in the accelerated maturation of osteoclast precursor cells (Zhou et al., 2008), a signalling which is”
BackgroundInfluentialXia, W.-F., Tang, F.-L., Xiong, L., Xiong, S., Jung, J.-U., Lee, D., Li, X.-S., Feng, X., Mei, L., & Xiong, W.-C. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201207154 · Cited by 48 · see citing works
“Bone histomorphometric analyses were performed as previously described (Zhou et al., 2006, 2008; Cui et al., 2011).”
MethodSelf-citationRAGE and its ligands in bone metabolism
Xiong, W.-C. (2010) · Frontiers in Bioscience-Scholar · doi:10.2741/s185 · Cited by 45 · see citing works
Self-citationRoles of Toll-like Receptor Signaling in Inflammatory Bone Resorption
Tominari, T., Matsumoto, C., Tanaka, Y., Shimizu, K., Takatoya, M., Sugasaki, M., Karouji, K., Kasuga, U., Miyaura, C., Miyata, S., et al. (2024) · Biology · doi:10.3390/biology13090692 · Cited by 42 · see citing works
“Several DAMPs derived from dead cells have been reported to function as endogenous TLR4 ligands, including high-mobility group box 1 (HMGB1) and S100 proteins, which induce osteoclastic bone resorption [42–44].”
BackgroundMovilă, A., Ishii, T., Albassam, A., Wisitrasameewong, W., Howait, M., Yamaguchi, T., Ruiz‐Torruella, M., Bahammam, L. A., Nishimura, K., Dyke, T. E. V., et al. (2016) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2854 · Cited by 42 · see citing works
“Although it is true that the positive effects of HMGB1 on bone resorption are well established,((58)) the roles played by the HMGB1/MIF complex in the migration of OCPs and osteoclastogenesis are unknown.”
BackgroundProgress and Applications of Polyphosphate in Bone and Cartilage Regeneration
Wang, Y., Li, M., Li, P., Teng, H., Fan, D., Du, W., & Guo, Z. (2019) · BioMed Research International · doi:10.1155/2019/5141204 · Cited by 44 · see citing works
“The interaction between RANKL produced by osteoblasts and its receptor RANK can induce (pre)osteoclasts differentiation [22, 64].”
BackgroundHMGB1 Localization during Experimental Periodontitis
Nogueira, A. V. B., de Souza, J. A. C., de Molon, R. S., Pereira, E. D. S. M., de Aquino, S. G., Giannobile, W. V., & Cirelli, J. A. (2014) · Mediators of Inflammation · doi:10.1155/2014/816320 · Cited by 40 · see citing works
“In vivo studies have shown similar results indicating that, in the presence of extracellular HMGB1, RANKL is able to induce more evident osteoclastogenesis [7].”
BackgroundResultActivation of cannabinoid receptors promote periodontal cell adhesion and migration
Liu, C., Qi, X., Alhabeil, J. A., Lu, H., & Zhou, Z. (2019) · Journal Of Clinical Periodontology · doi:10.1111/jcpe.13190 · Cited by 40 · see citing works
Self-citationPYK2 interacts with MyD88 and regulates MyD88-mediated NF-κB activation in macrophages
Xi, C.-X., Xiong, F., Zhou, Z., Mei, L., & Xiong, W. (2009) · Journal of Leukocyte Biology · doi:10.1189/jlb.0309125 · Cited by 38 · see citing works
“in 5% CO2 as previously described [17].”
Self-citationEarly stage blockade of the alarmin HMGB1 reduces cartilage destruction in experimental OA
Aulin, C., Lassacher, T. M., Palmblad, K., & Harris, H. E. (2020) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2020.01.003 · Cited by 38 · see citing works
The Role of Oxidative Stress in Aseptic Loosening of Total Hip Arthroplasties
Steinbeck, M. J., Delaney, L. J., Parvizi, J., & Freeman, T. A. (2013) · The Journal of Arthroplasty · doi:10.1016/j.arth.2013.09.001 · Cited by 37 · see citing works
“Finally, HMGB1 was evaluated, as it is an oxidative stress responsive protein required for RANKL-induced osteoclastogenesis [31].”
Martinotti, S., Patrone, M., Manfredi, M., Gosetti, F., Pedrazzi, M., Marengo, E., & Ranzato, E. (2016) · Journal of Cellular Biochemistry · doi:10.1002/jcb.25549 · Cited by 37 · see citing works
Irradiation‐induced osteocyte damage promotes HMGB1‐mediated osteoclastogenesis in vitro
He, F., Bai, J., Wang, J., Zhai, J., Tong, L., & Zhu, G. (2019) · Journal of Cellular Physiology · doi:10.1002/jcp.28351 · Cited by 37 · see citing works
“Moreover, extracellular HMGB1 has proved to support the generation of osteoclasts (Zhou et al., 2008).”
BackgroundChen, Y., Wang, Y., Tang, R., Yang, J., Dou, C., Dong, Y., Sun, D., Zhang, C., Zhang, L., Tang, Y., et al. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-2612-z · Cited by 37 · see citing works
HMGB1 Induces Secretion of Matrix Vesicles by Macrophages to Enhance Ectopic Mineralization
Chen, Q., Bei, J.-J., Liu, C., Feng, S.-B., Zhao, W.-B., Zhou, Z., Yu, Z.-P., Du, X.-J., & Hu, H.-Y. (2016) · PLoS ONE · doi:10.1371/journal.pone.0156686 · Cited by 38 · see citing works
“HMGB1, a nuclear protein released from stressed cells, has been indicated as a bone-active cytokine [17] and involved in ossification, arthritis and ectopic mineralization pathogenesis [18, 31].”
BackgroundSelf-citationFumimoto, R., Sakai, E., Yamaguchi, Y., Sakamoto, H., Fukuma, Y., Nishishita, K., Okamoto, K., & Tsukuba, T. (2012) · Journal of Pharmacological Sciences · doi:10.1254/jphs.11212fp · Cited by 36 · see citing works
Okui, T., Hiasa, M., Ryumon, S., Ono, K., Kunisada, Y., Ibaragi, S., Sasaki, A., Roodman, G. D., White, F. A., & Yoneda, T. (2020) · Journal of bone oncology · doi:10.1016/j.jbo.2020.100330 · Cited by 34 · see citing works
“A previous study described that HMGB1 increases RANKLinduced osteoclastogenesis via activating RAGE, but not TRL4, signaling [34].”
BackgroundResultPullerits, R., Forsblad‐d’Elia, H., Tarkowski, A., & Carlsten, H. (2009) · Lara D. Veeken · doi:10.1093/rheumatology/kep079 · Cited by 33 · see citing works
Davis, H. M., Valdez, S., Gomez, L., Malicky, P., White, F. A., Subler, M. A., Windle, J. J., Bidwell, J. P., Bruzzaniti, A., & Plotkin, L. I. (2019) · Journal of Cellular Biochemistry · doi:10.1002/jcb.28932 · Cited by 31 · see citing works
“In osteoclasts, HMGB1‐RAGE signaling regulates RANKL‐induced osteoclast differentiation and activity.(25) Further, epidermal growth factor‐mediated HMGB1 release induces RANK expression via CD68 in patients with autoimmune disease, suggesting that extracellular HMGB1 promotes osteoclast differentiation in human diseas…”
BackgroundDeng, Z., Ren, Y., Park, M. S., & Kim, H. K. W. (2021) · Bone · doi:10.1016/j.bone.2021.116215 · Cited by 32 · see citing works
The Load-Bearing Mechanosome Revisited
Bidwell, J. P., & Pavalko, F. M. (2010) · Clinical Reviews in Bone and Mineral Metabolism · doi:10.1007/s12018-010-9075-1 · Cited by 32 · see citing works
“RANKL stimulates HMGB1 release from macrophages [86] and PTH attenuates the release of HMGB1 from osteoblasts by repressing apoptosis [87].”
BackgroundLiou, S., Hsu, J., Lin, I., Ho, M., Hsu, P.-C., Chen, L., Chen, I., & Yeh, J. (2013) · PLoS ONE · doi:10.1371/journal.pone.0069468 · Cited by 29 · see citing works
“It has been demonstrated that release of extracellular HMGB1 can be induced by RANKL during an early stage of differentiation from BMMs into osteoclasts, and HMGB1 is believed as a critical mediator participating in RANKL-induced and integrin-dependent osteoclastogenesis [25].”
BackgroundInfluentialXiong, L., Xia, W.-F., Tang, F.-L., Pan, J., Mei, L., & Xiong, W. (2016) · EBioMedicine · doi:10.1016/j.ebiom.2016.05.028 · Cited by 27 · see citing works
“Bonehistomorphometric analyseswere carried out as previously described (Cui et al., 2010; Xia et al., 2013a; Xia et al., 2013b; Zhou et al., 2008; Zhou et al., 2006).”
MethodSelf-citationFrom death to birth: how osteocyte death promotes osteoclast formation
Zhao, W., Qian, J., Li, J., Su, T., Deng, X., Fu, Y., Liang, X., & Cui, H. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1551542 · Cited by 26 · see citing works
“HMGB1 can also directly act on OCPs and osteoclasts to induce osteoclast differentiation through RAGE and TLR4 activation (13).”
InfluentialtBHQ Suppresses Osteoclastic Resorption in Xenogeneic‐Treated Dentin Matrix‐Based Scaffolds
Sun, J.-J., Li, J., Li, H., Yang, H.-F., Chen, J.-L., Yang, B., Huo, F., Guo, W.-H., & Tian, W. (2017) · Advanced Healthcare Materials · doi:10.1002/adhm.201700127 · Cited by 23 · see citing works
Yamamoto, M., Sakiyama, K., Kitamura, K., Yamamoto, Y., Takagi, T., Sekiya, S., Watanabe, G., Taniguchi, S., Ogawa, Y., Ishizuka, S., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063006 · Cited by 27 · see citing works
HMGB1‐induced inflammatory response promotes bone healing in murine tooth extraction socket
Aoyagi, H., Yamashiro, K., Yoshihara‐Hirata, C., Ideguchi, H., Yamasaki, M., Kawamura, M., Yamamoto, T., Kochi, S., Wake, H., Nishibori, M., et al. (2018) · Journal of Cellular Biochemistry · doi:10.1002/jcb.26710 · Cited by 27 · see citing works
“Recently, Xue et al reported that recombinant HMGB1 in gelatin sponge scaffolds combined with mesenchymal stem cell sheets accelerates bone fracture healing.(9) In a future study, we will try to use the recombinantHMGB1protein to examinewhether it promotes bone healing in the tooth extraction socket.”
BackgroundPARP1 Hinders Histone H2B Occupancy at the NFATc1 Promoter to Restrain Osteoclast Differentiation
Wang, C., Xiao, J., Nowak, K., Gunasekera, K., Alippe, Y., Speckman, S., Yang, T., Kress, D., Abu‐Amer, Y., Hottiger, M. O., et al. (2019) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3927 · Cited by 23 · see citing works
“Other modified proteins included PARP1 itself, PARP14, heterogeneous ribonucleoproteins (hnRNPs), and high-mobility group box 1 (HMGB1), a well-characterized stimulator of OC formation.((73)) Western blot analysis using H2B antibody revealed no changes in the global levels of ADP-ribosylated H2B between macs and pOCs,…”
BackgroundSelf-citationRAGE supports parathyroid hormone-induced gains in femoral trabecular bone
Philip, B. K., Childress, P., Robling, A. G., Heller, A., Nawroth, P. P., Bierhaus, A., & Bidwell, J. P. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00564.2009 · Cited by 26 · see citing works
“Our comprehensive longitudinal analysis of the Rage-KO mouse during anabolic PTH treatment reveals a more complex skeletal phenotype than reported previously (11, 38) and suggests deficits in both the osteogenic and osteoclastic arms of skeletal homeostasis, which is consistent with recent studies showing a role for R…”
BackgroundResultInfluentialrhHMGB1 drives osteoblast migration in a TLR2/TLR4- and NF-κB-dependent manner
Li, M.-J., Li, F., Xu, J., Liu, Y., Hu, T., & Chen, J.-T. (2016) · Bioscience Reports · doi:10.1042/bsr20150239 · Cited by 26 · see citing works
Hou, C., Luan, L., & Ren, C. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.11.083 · Cited by 25 · see citing works
Baicalin positively regulates osteoclast function by activating MAPK/Mitf signalling
Lu, L., Rao, L., Jia, H., Chen, J., Lu, X., Yang, G., Li, Q., Lee, K. K., & Yang, L. (2017) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13066 · Cited by 24 · see citing works
S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis
Kim, H., Kim, S. I., Kim, S. I., Kim, H. J., Ryu, B. Y., Chung, J., Lee, Z. H., & Kim, H. (2019) · Bone Research · doi:10.1038/s41413-019-0068-5 · Cited by 24 · see citing works
Lin, Y., Zheng, G. H., Liu, H., Wang, P., Yuan, W.-Q., Zhang, Y., Peng, X., Li, G.-J., Wu, Y., & Shen, H. (2023) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2023.05.007 · Cited by 24 · see citing works
“Previous studies have shown that the expression of HMGB1 is upregulated during the osteoclast differentiation of CD14þ PBMCs induced by RANKL in vitro, and the recombination of the actin cytoskeleton of osteoclasts is regulated by the receptor for advanced glycation end products (RAGE) [34].”
BackgroundGuo, J.-P., Pan, J., Xiong, L., Xia, W.-F., Cui, S., & Xiong, W. (2015) · PLoS ONE · doi:10.1371/journal.pone.0139395 · Cited by 24 · see citing works
“ThemicroCT analysis was carried out as described previously [17, 18].”
MethodInfluentialSelf-citationWolf, M. F., Lossdörfer, S., Küpper, K., & Jäger, A. (2013) · European Journal of Orthodontics · doi:10.1093/ejo/cjt037 · Cited by 23 · see citing works
The RAGE signaling in osteoporosis
Zhou, J., Liu, S., Bi, S., Kong, W., Qian, R., Xie, X., Zeng, M., Jiang, X., Liao, Z., Shuai, M., et al. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115044 · Cited by 22 · see citing works
Wolf, M. F., Lossdörfer, S., Craveiro, R. B., Götz, W., & Jäger, A. (2013) · Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie · doi:10.1007/s00056-013-0167-7 · Cited by 22 · see citing works
Roles of High Mobility Group Box 1 in Cardiovascular Calcification
Chen, Q., Wang, Z., Chen, L., & Hu, H. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000477591 · Cited by 22 · see citing works
Sakamoto, Y., Okui, T., Yoneda, T., Ryumon, S., Nakamura, T., Kawai, H., Kunisada, Y., Ibaragi, S., Masui, M., Ono, K., et al. (2020) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2020.07.120 · Cited by 20 · see citing works
“Some reports indicated that HMGB1 directly promotes maturation of osteoclasts independent of RANKL signaling [12].”
BackgroundInfluentialSoluble CD93 lectin-like domain sequesters HMGB1 to ameliorate inflammatory diseases
Huang, S., Kuo, C., Shiao, S.-Y., Shen, C., Lee, F.-T., Chang, B.-I., Hsu, J., Wu, H., Yeh, J., & Lai, C. (2023) · Theranostics · doi:10.7150/thno.84935 · Cited by 20 · see citing works
“Immunofluorescence staining showed that RANKL stimulation substantially accentuated the staining of HMGB1 that was colocalized with F-actin (Figure S5B), a prerequisite cytoplasmic structure for osteoclast bone resorption [34].”
BackgroundResultInfluentialLiu, B., Gan, X., Zhao, Y., Yu, H., Gao, J., & Yu, H. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/1703709 · Cited by 20 · see citing works
“Moreover, studies have shown that in osteoclast precursor cells, RAGE appears to be required for integrin signaling and the cross-talk between HMGB1 and integrin signaling [39].”
BackgroundYamaguchi, Y., Sakai, E., Sakamoto, H., Fumimoto, R., Fukuma, Y., Nishishita, K., Okamoto, K., & Tsukuba, T. (2012) · Journal of Applied Toxicology · doi:10.1002/jat.2827 · Cited by 19 · see citing works
“…HMGB1, which acts as a proinflammatory cytokine, can bind to cell-surface receptors such as the receptor for advanced glycation end products and Toll-like receptors 2 and 4, and modulate differentiation of OCL precursors in the presence of RANKL (Yamoah et al., 2008; Zhou et al., 2008).”
BackgroundResultInfluentialMechanisms of Osteoinduction/Chondroinduction by Demineralized Bone
Glowacki, J., Zhou, S., & Mizuno, S. (2009) · Journal of Craniofacial Surgery · doi:10.1097/scs.0b013e3181928077 · Cited by 18 · see citing works
Myeloid thrombomodulin lectin-like domain inhibits osteoclastogenesis and inflammatory bone loss
Cheng, T., Lai, C., Shieh, S.-J., Jou, Y.-B., Yeh, J., Yang, A.-L., Wang, Y., Wang, C., Chen, C., Shi, G.-Y., et al. (2016) · Scientific Reports · doi:10.1038/srep28340 · Cited by 18 · see citing works
Self-citationTakahashi, T., Katsuta, S., Tamura, Y., Nagase, N., Suzuki, K. W., Nomura, M., Tomatsu, S., Miyamoto, K., & Kobayashi, S. (2013) · Molecular Medicine · doi:10.2119/molmed.2012.00309 · Cited by 18 · see citing works
Deltamethrin inhibits osteoclast differentiation via regulation of heme oxygenase-1 and NFATc1
Sakamoto, H., Sakai, E., Fumimoto, R., Yamaguchi, Y., Fukuma, Y., Nishishita, K., Okamoto, K., & Tsukuba, T. (2012) · Toxicology in Vitro · doi:10.1016/j.tiv.2012.05.005 · Cited by 17 · see citing works
Nishioku, T., Toshiki, K. U. B. O., KAMADA, T., Okamoto, K., Tsukuba, T., Uto, T., & Shoyama, Y. (2020) · Biomedical Research · doi:10.2220/biomedres.41.269 · Cited by 17 · see citing works
“It has been shown that extracellular HMGB1 interacts with RAGE during osteoclastogenesis (Zhou et al. 2008).”
BackgroundInfluentialNishioku, T., Kawamoto, M., Okizono, R., Sakai, E., Okamoto, K., & Tsukuba, T. (2020) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2020.05.088 · Cited by 16 · see citing works
Wolf, M. F., Lossdörfer, S., Craveiro, R. B., & Jäger, A. (2013) · Innate Immunity · doi:10.1177/1753425913505121 · Cited by 16 · see citing works
“osteoclastic differentiation.(21) Sha et al.”
Kim, H. K. W., Park, M. S., do Monte, F. A., Gokani, V., Aruwajoye, O. O., & Ren, Y. (2021) · Journal of Bone and Joint Surgery · doi:10.2106/jbjs.20.00578 · Cited by 15 · see citing works
Li, M., Ong, C. Y., Langouët-Astrié, C. J., Tan, L., Verma, A., Yang, Y., Zhang, X., Shah, D. K., Schmidt, E. P., & Xu, D. (2022) · eLife · doi:10.7554/elife.71403 · Cited by 15 · see citing works
Hui, P., Zhou, S., Cao, C., Zhao, W., Zeng, L., & Rong, X. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1195567 · Cited by 14 · see citing works
“HMGB1 has been demonstrated to play an essential role in autoimmune diseases such as rheumatoid arthritis (RA), as well as in inflammatory events (Zhou et al., 2008).”
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Monir, A., Mukaibo, T., Abdelaal, A., Nodai, T., Munemasa, T., Kondo, Y., Masaki, C., El-Shair, M. A., Matsuo, K., & Hosokawa, R. (2021) · Scientific Reports · doi:10.1038/s41598-021-88195-7 · Cited by 14 · see citing works
Bone matrix quality in a developing high-fat diet mouse model is altered by RAGE deletion
Stephen, S. J., Bailey, S., D'Erminio, D. N., Krishnamoorthy, D., Iatridis, J. C., & Vashishth, D. (2022) · Bone · doi:10.1016/j.bone.2022.116470 · Cited by 14 · see citing works
Chang, L., Lai, C., Kuo, C., Chang, B.-I., Wu, H., & Cheng, T. (2021) · Journal of Periodontology · doi:10.1002/jper.20-0732 · Cited by 14 · see citing works
Turner, M. E., Bartoli‐Leonard, F., & Aïkawa, E. (2022) · Immunological Reviews · doi:10.1111/imr.13134 · Cited by 14 · see citing works
Yang, X. Y., Gandhi, C., Rahman, M. M., Appleford, M. R., Sun, L.-W., & Wang, X. (2015) · Calcified Tissue International · doi:10.1007/s00223-015-0042-1 · Cited by 13 · see citing works
- Authors
- Zhou, Z., Han, J.-Y., Xi, C.-X., Xie, J.-X., Feng, X., Wang, C.-Y., Mei, L., & Xiong, W.-C.
- Affiliations
- Augusta University (US)
- University of Alabama at Birmingham (US)
- Corresponding author
- Xiong, Wen-Cheng
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-07-01
- Volume
- 23
- Issue
- 7
- Pages
- 1084-1096
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- PMC
- PMC2679382
- OpenAlex
- W2126202075
- Cited by
- 160
- References
- 43
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 12 · 2020: 14 · 2019: 15 · 2018: 8 · 2017: 8 · 2016: 11 · 2015: 7 · 2014: 6 · 2013: 16 · 2012: 5
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Journal of Bone and Mineral Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR048120, AR048120)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- HMGB1, RANKL, osteoclastogenesis, RAGE, receptor for advanced glycation end products, macrophages, bone resorption, actin cytoskeleton remodeling, integrin signaling, inflammatory bone loss, extracellular HMGB1
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Base Sequence, Cell Division, Fluorescent Antibody Technique, Osteoclasts, Receptors, Immunologic, Blotting, Western, DNA Primers, Mice, Knockout, HMGB1 Protein, Mice, RANK Ligand
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