Cited by 172Bone Metabolism and DiseasesAdvanced Glycation End Products researchImmune Response and Inflammation

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

HMGB1 Regulates RANKL-Induced Osteoclastogenesis in a Manner Dependent on RAGE

Open access

Zhou, Zheng, Han, Jun-Yan, Xi, Cai-Xia, Xie, Jian-Xin, Feng, Xu, Wang, Cong-Yi, Mei, Lin, Xiong, Wen-Cheng·2008·Journal of Bone and Mineral Research

DOI 10.1359/jbmr.080234PMC PMC2679382

Open this paper in CoChat — free account

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1359/jbmr.080234

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Osteoclast differentiation and activation
Boyle, W. J., Simonet, W. S., & Lacey, D. L. (2003) · Nature · doi:10.1038/nature01658 · Cited by 6,670
Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.
Lacey, D. L., Timms, E., Tan, H.-L., Kelley, M. J., Dunstan, C. R., Burgess, T., Elliott, R., Colombero, A., Elliott, G., Scully, S., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81569-x · Cited by 5,439
Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL
Yasuda, H., Shima, N., Nakagawa, N., Yamaguchi, K., Kinosaki, M., Mochizuki, S.-I., Tomoyasu, A., Yano, K., Goto, M., Murakami, A., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.7.3597 · Cited by 4,224
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal
Lotze, M. T., & Tracey, K. J. (2005) · Nature reviews. Immunology · doi:10.1038/nri1594 · Cited by 2,490
Involvement of Toll-like Receptors 2 and 4 in Cellular Activation by High Mobility Group Box 1 Protein
Park, J. S., Svetkauskaite, D., He, Q., Kim, J., Strassheim, D., Ishizaka, A., & Abraham, E. H. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m306793200 · Cited by 1,582
TNF-α induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand
Lam, J., Takeshita, S., Barker, J. E., Kanagawa, O., Ross, F. P., & Teitelbaum, S. L. (2000) · Journal of Clinical Investigation · doi:10.1172/jci11176 · Cited by 1,440 · cited 1×
“text, because release of HMGB1 is elicited by lipopolysaccharide and multiple inflammatory mediators (IL-1, TNF , interferon- and - ), we propose that the HMGB1–RAGE interaction could represent a final common pathway in inflammation-associated bone resorption.((9,35,39))”
Background
The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses
Schmidt, A. M., Yan, S. D., Yan, S. F., & Stern, D. M. (2001) · Journal of Clinical Investigation · doi:10.1172/jci14002 · Cited by 1,256
Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion
Bonaldi, T., Talamo, F., Scaffidi, P., Ferrera, D., Porto, A., Bachi, A., Rubartelli, A., Agresti, A., & Bianchi, M. E. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg516 · Cited by 1,252
Cholinergic agonists inhibit HMGB1 release and improve survival in experimental sepsis
Wang, H., Liao, H., Ochani, M., Justiniani, M., Lin, X., Yang, L., Al-Abed, Y., Wang, H., Metz, C., Miller, E. J., et al. (2004) · Nature Medicine · doi:10.1038/nm1124 · Cited by 1,170

Show all 43 references

Sorted by citations

Items 101–172 of 172

Serial Passaging of RAW 264.7 Cells Modulates Intracellular AGE Formation and Downregulates RANKL-Induced In Vitro Osteoclastogenesis
Lucy, T. T., Mamun-Or-Rashid, A. N. M., Yagi, M., & Yonei, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23042371 · Cited by 12
“RAGE was reported to play vital role on cell–cell fusion by binding with extracellular HMGB1 [33], and thereby induce osteoclastogenesis and its function.”
BackgroundResult
High mobility group box protein 1—A prognostic marker for structural joint damage in 10-year follow-up of patients with juvenile idiopathic arthritis
Pullerits, R., Schierbeck, H., Uibo, K., Liivamägi, H., Tarraste, S., Talvik, T., Sundberg, E., & Pruunsild, C. (2016) · Seminars in Arthritis and Rheumatism · doi:10.1016/j.semarthrit.2016.08.017 · Cited by 11
Inorganic Polyphosphates: Biologically Active Biopolymers for Biomedical Applications
Wang, X., Schröder, H. C., Schloßmacher, U., & Müller, W. E. G. (2013) · Progress in molecular and subcellular biology · doi:10.1007/978-3-642-41004-8_10 · Cited by 12
“RANKL stimulates osteoclast precursor cells to differentiate into mature osteoclasts (Zhou et al. 2008), while the maturation of osteoblasts from their precursor cells is promoted by bone morphogenetic protein 2 (BMP-2) (Chen et al.”
Background
The complex relationship between bone remodeling and the physical and material properties of bone
Burr, D. B. (2014) · Osteoporosis International · doi:10.1007/s00198-014-2970-4 · Cited by 11
“However, they also can stimulate osteoclast differentiation and activation through the RANKL pathway [9].”
Background
Levels of high-mobility group box-1 in gingival crevicular fluid in nonsmokers and smokers with chronic periodontitis
Lin, Y.-C., Wu, C., Chang, L., Chen, C.-C., Chen, H., Lai, Y., & Hung, S. (2017) · Journal of the Formosan Medical Association · doi:10.1016/j.jfma.2017.01.006 · Cited by 11
“In addition, HMGB1 also regulates receptor activator of nuclear factor-kB ligand (RANKL)-induced osteoclastogenesis in vitro and in vivo.(25) HMGB1 can be found in gingival tissues and GCF.”
BackgroundInfluential
RAGE Deficiency Impairs Bacterial Clearance in Murine Staphylococcal Sepsis, but Has No Significant Impact on Staphylococcal Septic Arthritis
Mohammad, M., Na, M., Welin, A., Svensson, M. N. D., Ali, A. M., Jin, T., & Pullerits, R. (2016) · PLoS ONE · doi:10.1371/journal.pone.0167287 · Cited by 10
“Furthermore, a previous study indicated that HMGB1 via RAGE regulates and enhances the osteoclastogenesis, suggesting that RAGE plays a vital role in the HMGB1 mediated osteoclastogenesis in vivo [39].”
Background
Antidiabetic Agents and Bone Quality: A Focus on Glycation End Products and Incretin Pathway Modulations
Zaki, M. K., Abed, M. N., & Alassaf, F. A. (2024) · Journal of Bone Metabolism · doi:10.11005/jbm.2024.31.3.169 · Cited by 9
“[14 ] Additionally, it appears that RANKL encourages the expression of RAGE and, as a result, osteoclast differentiation.”
Background
Involvement of Noncoding RNAs in the Differentiation of Osteoclasts
Zhao, Y., Jia, L., Zheng, Y., & Li, W. (2020) · Stem Cells International · doi:10.1155/2020/4813140 · Cited by 9
“HMGB1-RAGE signaling plays important roles in regulating actin cytoskeleton reorganization in osteoclasts, thereby participating in RANKL-induced osteoclastogenesis [165].”
Background
Relationships between High-mobility Group Protein B1 and Triggering Receptor Expressed on Myeloid Cells Concentrations in Gingival Crevicular Fluid and Chronic Periodontitis.
Paknejad, M., Sattari, M., roozbahani, Z., Ershadi, M., & Mehrfard, A. (2016) · PubMed · Cited by 9
DAMPs, PAMPs, NLRs, RIGs, CLRs and TLRs – Understanding the Alphabet Soup in the Context of Bone Biology
Carroll, K. A., Sawden, M., & Sharma, S. (2025) · Current Osteoporosis Reports · doi:10.1007/s11914-024-00900-3 · Cited by 10
“HMGB1 engages TLR4 to stimulate pro-inflammatory cytokine and RANK signaling, promoting osteoclastogenesis in precursor cells [24].”
Ginseng (Panax ginseng) leaf extract modulates the expression of heme oxygenase-1 to attenuate osteoclast differentiation
Lee, H. G., Hur, J., Won, J. P., & Seo, H. G. (2024) · Fitoterapia · doi:10.1016/j.fitote.2024.105831 · Cited by 8
HMGB1 as an emerging key modulator of bone remodeling: a narrative review
Tang, J., Li, M., & Huang, L. C. (2025) · Stem Cell Research & Therapy · doi:10.1186/s13287-025-04543-8 · Cited by 7
“Subsequently, HMGB1 binds to the RAGE receptor on the membrane of OCPs, facilitating actin cytoskeleton remodeling and actin ring formation, which leads to osteoclast maturation [16, 49].”
Influential
HMGB1 orchestrates tumor-osteoclast crosstalk to drive bone metastasis in hepatocellular carcinoma
Chen, Y.-Z., Xu, D., Jia, Y.-X., Ma, J., & Xiang, Z. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-08037-6 · Cited by 6
“Within the bone microenvironment, HMGB1 interacts with toll-like receptor 4 (TLR4) to regulate osteoclast activation and modulate macrophage responses, processes implicated in osteolytic bone destruction [22 – 24].”
HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · BMC Genomics · doi:10.1186/s12864-024-10204-6 · Cited by 6
“HMGB1-promoted genes are highly enriched in osteoclast differentiation, consistent with the reported function of HMGB1 in regulating osteoclast genesis in a manner dependent on RAGE [46].”
Background
Orthodontic tooth movement and HMGB1
Kanzaki, H., & Nakamura, Y. (2018) · Journal of Oral Biosciences · doi:10.1016/j.job.2018.03.002 · Cited by 6
Intercellular junctions and cell–cell communication in the skeletal system
Stains, J. P., Fontana, F., & Civitelli, R. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-814841-9.00018-x · Cited by 6
High-mobility Group Box 1 Is Associated with the Inflammatory Infiltration and Alveolar Bone Destruction in Rats Experimental Periapical Lesions
Liu, L., Deng, J., Ji, Q., & Peng, B. (2017) · Journal of Endodontics · doi:10.1016/j.joen.2016.11.014 · Cited by 5
“Thus, extracellular HMGB1 is necessary for RANKL-induced osteoclastogenesis; osteoclast markers including calcitonin R, cathepsin K, and matrix metallproteinase-9; and integrin activation–dependent actin ring formation (9).”
Background
Trabecular Bone Deficit and Enhanced Anabolic Response to Re-Ambulation after Disuse in Perlecan-Deficient Skeleton
Parajuli, A., Pei, S., Zhao, H., Martinez, J. R., Lu, X. L., Liu, X. S., Farach‐Carson, M. C., Kirn‐Safran, C. B., & Wang, L. (2020) · Biomolecules · doi:10.3390/biom10020198 · Cited by 5
“GAGs inhibit the adherence and spreading of osteoclasts and their precursors [33], and heparan sulfate side chains of perlecan could sequester and prevent the high-mobility group box 1 protein released by bone marrow macrophages from promoting the differentiation of pre-osteoclasts [34].”
Background
Genetic and Epigenetic Aspects of Bone Development
O’Connor, R. D., Farach‐Carson, M. C., & Schanen, N. C. (2010) · Springer eBooks · doi:10.1007/978-1-84882-822-3_1 · Cited by 5
“A subsequent study [188] reported that HMGB1, a high-mobility group protein, could act as an autocrine ligand for RAGE.”
Background
Endothelial Precursor Cells and CRP on the RAGE: Activation or Cell Death?
Yan, S. D., Bierhaus, A., Nawroth, P. P., & Stern, D. M. (2009) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e31819d6188 · Cited by 5
“For example, in osteoclast development, it has been shown that receptor activator of NF-kB (RANK) ligand causes release of HMGB1 from macrophages, which stimulates RAGE and subsequently triggers a pathway leading to osteoclast differentiation.(14,15) In the current circumstance (CRP and EPCs), we speculate that CRP ca…”
Background
HMGB1 couples LEF1 to regulate B cell immunity
Chen, Q., Zhang, Z., Xiang, N., Luo, L., Dai, X., Kang, D., Yang, L., Zhu, Y., Chang, J., Jing, Y., et al. (2025) · JCI Insight · doi:10.1172/jci.insight.187002 · Cited by 4
“HMGB1 also plays a role in cytoskeletal dynamics by inducing actin reorganization in various cell types (13).”
In-vitro analysis of resorption processes following high hydrostatic pressure treatment of human trabecular bone
Waletzko‐Hellwig, J., Pohl, C., Loeffler, H., Dau, M., Schlosser, M., Bader, R., & Klinder, A. (2022) · Materials & Design · doi:10.1016/j.matdes.2022.111539 · Cited by 4
Stress overload‐induced periodontal remodelling coupled with changes in high mobility group protein B1 during tooth movement: an in‐vivo study
Zou, Y., Xu, L., & Lin, H. (2019) · European Journal Of Oral Sciences · doi:10.1111/eos.12644 · Cited by 4
S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Ceglie, I. D., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Arthritis Research & Therapy · doi:10.1186/s13075-021-02602-y · Cited by 4
Salivary and serum levels of high mobility group box protein 1 in periodontitis: a cross-sectional observational study
Öner, F., Özgenç, G., Aslan, H., Guzeltan, O., & Karasu, Y. Ö. (2025) · BMC Oral Health · doi:10.1186/s12903-025-06954-8 · Cited by 3
“HMGB1 has osteoclastogenic characteristics, initiating osteoclast differentiation [15] and regulating receptor activator of nuclear factor of kappa beta ligand (RANKL)-mediated osteoclastic activity [16] through RAGE activation [15, 16].”
Microenvironmental Drivers of Bone Disease in Multiple Myeloma: Oxidative Stress, Sterile Inflammation, Autophagy–Lysosomal Remodeling, and the Iron–Lipid Peroxidation Axis
Nasso, M. E., Bottaro, A., Fazio, M., Stagno, F., Gangemi, S., & Allegra, A. (2026) · Biomolecules · doi:10.3390/biom16050710 · Cited by 3
“…a reduced activation threshold in osteoclast precursors, driven by RAGE-and TLR-dependent amplification of NF-κ B and MAPK signaling, which synergizes with RANKL to sustain NFATc1 induction and osteoclast differentiation while concomitantly suppressing osteoblast lineage commitment [25–27].”
Systemic and Local Cytokines Profile Determine Severity and Prognosis in Human Septic Arthritis
González-Chapa, J. A., Peña‐Martínez, V. M., Vílchez-Cavazos, J. F., Salinas-Carmona, M. C., & Rosas-Taraco, A. G. (2021) · Archives of Medical Research · doi:10.1016/j.arcmed.2021.10.004 · Cited by 3
Mechanism for the Development of Bone Disease in Diabetes: Increased Oxidative Stress and Advanced Glycation End Products
Yamagishi, S. (2016) · Springer eBooks · doi:10.1007/978-4-431-55720-3_5 · Cited by 3
“Moreover, highmobility group box 1 (HMGB1), a nonhistone nuclear protein and one of the ligands of RAGE, has been shown to enhance RANKL-induced osteoclastogenesis both in cell culture and animal model [46].”
Background
Expression of the Inflammatory Molecule HMGB1 in Human Osteosarcoma and its Clinical Relevance
Li, B., Jiang, S.-D., Zheng, X.-F., Ni, B.-B., Yang, Y., Chen, J., Chen, K., & Ls, J. (2013) · European Journal of Inflammation · doi:10.1177/1721727x1301100107 · Cited by 3
Introduction to the Global Scenario of Marine Sponge Research
Bramhachari, P. V., Ehrlich, H., & Pallela, R. (2016) · Springer eBooks · doi:10.1007/978-81-322-2794-6_1 · Cited by 3
High-Mobility Group Box 1 Expression in Mandibular Bone Cells of Experimental Periodontitis
Arina, Y. M. D., Rubianto, M., Ferdiansyah, F., Sudiana, I. K., Rahayu, R. P., & Notobroto, H. B. (2019) · Contemporary Clinical Dentistry · doi:10.4103/ccd.ccd_907_18 · Cited by 3
“[24] The previous study has been demonstrated that HMGB1 molecules have a synergistic effect with RANKL to regulate osteoclastogenesis.[25] Based on previous study, the HMGB1 alters osteoblast expression of RANKL or OPG[26] and participates in osteoclastogenesis process.”
BackgroundInfluential
Coffee and Bone Metabolism
Sakai, E., & Tsukuba, T. (2014) · Coffee in Health and Disease Prevention · doi:10.1016/b978-0-12-409517-5.00096-6 · Cited by 3
High-mobility group box 1 is a promising diagnostic and therapeutic monitoring biomarker in Cancers: A review
Richard, S. A. (2018) · AIMS molecular science · doi:10.3934/molsci.2018.4.183 · Cited by 4
Porphyromonas gingivalis –Derived Virulence Lipids Accelerate Osteoclastogenesis Independently of High Mobility Group Box Protein‐1 Canonical Signaling
Yamada, C., Peng, G., Johnson, J., Nusbaum, A., Sanz, N., AlQallaf, H., Nichols, F. C., & Movilă, A. (2025) · Molecular Oral Microbiology · doi:10.1111/omi.70015 · Cited by 2
“It was further reported that HMGB1 is released from RANKL-primed osteoclast precursors, playing a pivotal role in osteoclastogenesis (Zhou et al. 2008).”
Influential
HMGB-1 Levels in Painful Knee Arthroplasty: Is it Possible to Distingue Periprosthetic Joint Infection and Aseptic Loosening?
Rızvanoğlu, İ. H., Sakarya, B., Benlier, N., & Kökçü, F. (2023) · Indian Journal of Orthopaedics · doi:10.1007/s43465-023-00903-9 · Cited by 2
“reported that the increase in HMGB-1 was directly proportional to the degree of osteolytic severity in AL [36, 37].”
Background
Low Serum Level of the Endogenous Secretory Receptor for Advanced Glycation End Products (esRAGE) Is a Risk Factor for Prevalent Vertebral Fractures Independent of Bone Mineral Density in Patients with Type 2 Diabetes
Yamamoto, M., Yamaguchi, T., Yamauchi, M., & Sugimoto, T. (2010) · Diabetes Care · doi:10.2337/dc10-0109 · Cited by 2
“(3) suggests that HMGB1 may play a role in bone metabolism.”
Background
DYSREGULATION OF BONE METABOLISM DURING TYPE 2 DIABETES MELLITUS: ROLE OF TOLL-LIKE RECEPTOR-4 AND AUTOPHAGY
Rendina-Ruedy, E. (2015) · SHAREOK (University of Oklahoma; Oklahoma State University; Central Oklahoma University) · doi:10.13140/rg.2.1.5090.3208 · Cited by 2
Validation of the therapeutic potential of soluble CD93 lectin-like domain in arthritis and its inhibitory role in inflammatory osteolysis
Huang, S., Kuo, C., Wu, H., Sulistyowati, E., Lee, F.-T., Lai, C., & Yeh, J. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115533 · Cited by 1
Immunogene Zelltodmarker HMGB1 und sRAGE als neue prädiktive und prognostische Serum Biomarker bei Tumorerkrankungen/Immunogenic cell death markers HMGB1 and sRAGE as new predictive and prognostic serum biomarkers in cancer disease
Wittwer, C., & Holdenrieder, S. (2013) · Journal of Laboratory Medicine · doi:10.1515/labmed-2013-0005 · Cited by 1
Sessile Innate Immune Cells
Land, W. G. (2018) · Springer eBooks · doi:10.1007/978-3-319-78655-1_9 · Cited by 1
Magnolia kobus Extract Suppresses Porphyromonas gingivalis LPS-Induced Proinflammatory Cytokine and MMP Expression in HGF-1 Cells and Regulates Osteoclastogenesis in RANKL-Stimulated RAW264.7 Cells
Lee, H. J., Lee, S. J., Lee, S. K., Choi, B. K., Lee, D. R., Park, J.-H., & Oh, J. S. (2023) · Current Issues in Molecular Biology · doi:10.3390/cimb45060310 · Cited by 1
Dual cytokine inducing properties of HMGB1
Hreggvidsdottir, H. S. (2011) · Figshare · Cited by 1
Role of DAMPS on the modulation of macrophage response after classical biomaterial (Ti) implantation and its impact on the subsequent repair and osseointegration processes
Biguetti, C. C. (2018) · doi:10.11606/t.25.2018.tde-02102018-153955 · Cited by 1
“differentiation [25], proliferation and collagen synthesis by osteoblasts [26, 27] and angiogenesis [24, 28].”
Background
The role of inflammation and oxidative stress in total hip replacement revisions
Jablonowski, L. J., & Allen, F. D. (2011) · doi:10.17918/etd-3726 · Cited by 1
Genetic and pharmacologic modulation of RAGE rescues the diabetes-mediated impairments to bone at multiple length scalesPreprint
Broz, K. S., Hung, T., Walk, R. E., LoTempio, S., Flores, K. M., & Tang, S. Y. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.02.716153 · Cited by 1
Acute Coronary Syndrome: Pathological Findings by Means of Electron Microscopy, Advance Imaging in Cardiology
Behjati, M., & Moradi, I. (2012) · InTech eBooks · doi:10.5772/29985
Osteoblasts and Wnt signaling: Meeting report from the 30th Annual Meeting of the American Society for Bone and Mineral Research
Caverzasio, J. (2008) · IBMS BoneKEy · doi:10.1138/20080353
HMGB1 in inflammation - secretion and function
Wähämaa, H. (2008) · Figshare
Bone and Diabetes
Palermo, A., Naciu, A., Tabacco, G., D'Onofrio, L., & Napoli, N. (2018) · Springer eBooks · doi:10.1007/978-3-319-75110-8_10 · Cited by 2
Oral biosciences: The annual review 2018
Ohshima, H., & Amizuka, N. (2019) · Journal of Oral Biosciences · doi:10.1016/j.job.2019.01.003
Mechanisms of skeletal fragility in diabetes mellitus
Mizokami‐Stout, K., & Clines, G. A. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-820605-8.00003-6
HMGB1 and TLR4 as biomarkers for osteoporosis risk in type 2 diabetes mellitus: a cross-sectional study
Zhu, G., Kan, C., Cao, C., & Zhu, H. (2025) · BMC Endocrine Disorders · doi:10.1186/s12902-025-01998-x
“One plausible explanation is the role of HMGB1 in regulating actin cytoskeletal organization and integral linkage protein signaling via RAGE in bone marrow macrophages, participating in osteoclast generation in vitro and ex vivo [18].”
Additional file 1 of S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Di Ceglie, I., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Figshare · doi:10.6084/m9.figshare.15569238
Additional file 2 of S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Di Ceglie, I., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Figshare · doi:10.6084/m9.figshare.15569265
Additional file 12 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702674
Additional file 4 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702650
Additional file 3 of S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Di Ceglie, I., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Figshare · doi:10.6084/m9.figshare.15569268
Additional file 1 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25556497
Additional file 2 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25556658
Additional file 13 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702677
Additional file 14 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702680
Additional file 5 of S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Di Ceglie, I., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Figshare · doi:10.6084/m9.figshare.15569292
Additional file 7 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702659
Additional file 10 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702668
Additional file 3 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702647
Additional file 5 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702653
Additional file 9 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702665
Additional file 6 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702656
Additional file 8 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702662
Additional file 4 of S100A8/A9 is not essential for the development of inflammation and joint pathology in interleukin-1 receptor antagonist knockout mice
Di Ceglie, I., van Lent, P. L. E. M., Geven, E. J., Koenders, M. I., Blom, A. B., Vogl, T., Roth, J., & van den Bosch, M. H. J. (2021) · Figshare · doi:10.6084/m9.figshare.15569286
Additional file 11 of HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Liao, M., Cao, J., Chen, W., Wang, M., Jin, Z., Ye, J., Ren, Y., Wei, Y., Xue, Y., Chen, D., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26702671
Pathophysiology of bone quality changes in obese diabetics
Fröhlich, M., Jackuliak, P., Smaha, J., & Payer, J. (2021) · Clinical Osteology · doi:10.36290/clo.2021.013

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
ORCID: Zhou, Zheng
Feng, Xu
Wang, Cong-Yi
Mei, Lin
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
DOI: 10.1359/jbmr.080234
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

HMGB1 Regulates RANKL-Induced Osteoclastogenesis in a Manner Dependent on RAGE

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks