Evidence map›Paper›PMID 35879285›Full record

ArticleBone research2022

Dynamic changes in O-GlcNAcylation regulate osteoclast differentiation and bone loss via nucleoporin 153.

Yi-Nan Li, Chih-Wei Chen, Thuong Trinh-Minh, Honglin Zhu, Alexandru-Emil Matei, Andrea-Hermina Györfi, Frederic Kuwert, Philipp Hubel, Xiao Ding, Cuong Tran Manh and 11 more

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  3. Artificial intelligence virtual bone organoids (AIVBOs).Journal of orthopaedic translation · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 4 institutions in 3 countries.

Yi-Nan Li *Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0001-8934-9361
Chih-Wei Chen *Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Thuong Trinh-MinhDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Honglin ZhuDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Alexandru-Emil MateiDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Andrea-Hermina GyörfiDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Frederic KuwertDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Philipp HubelCore Facility Hohenheim, University of Hohenheim, Stuttgart, Germany.
Xiao DingDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Cuong Tran ManhDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Xiaohan XuDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Christoph LiebelDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Vladyslav FedorchenkoDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Ruifang LiangDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Kaiyue HuangDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Jens PfannstielCore Facility Hohenheim, University of Hohenheim, Stuttgart, Germany.
Min-Chuan HuangGraduate Institute of Anatomy and Cell biology, National Taiwan University College of Medicine, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-0704-3447
Neng-Yu LinGraduate Institute of Anatomy and Cell biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Andreas RammingDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Georg SchettDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0001-8740-9615
Jörg H W DistlerDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany. joerg.distler@uk-erlangen.de.ORCID http://orcid.org/0000-0001-7408-9333
Friedrich-Alexander-Universität Erlangen-Nürnberg · DENational Taiwan University · TWUniversity of Hohenheim · DECentral South University · CN

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) MASCARA program/ TP2 (01EC1903A)Deutsche Forschungsgemeinschaft (German Research Foundation) 324392634 (B04)Deutsche Forschungsgemeinschaft (German Research Foundation) DI 1537/14-1, DI 1537/17-1, DI 1537/20-1, DI 1537/22-1Deutsche Forschungsgemeinschaft (German Research Foundation) MA 9219/2-1Deutsche Forschungsgemeinschaft (German Research Foundation) RA 2506/3-1Deutsche Forschungsgemeinschaft (German Research Foundation) SFB CRC1181 (project C01)Friedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) 19-12-06-1-MateiFriedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) 21-07-23-1-GyörfiFriedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) A64Friedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) A79, A64Friedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) J40Friedrich Alexander University of Erlangen Nuremberg | Medizinische Fakultät, Friedrich-Alexander-Universität Erlangen-Nürnberg (Faculty of Medicine, Friedrich Alexander University of Erlangen Nuremberg) J82
6 · The paper itself

Abstract

Bone mass is maintained by the balance between osteoclast-induced bone resorption and osteoblast-triggered bone formation. In inflammatory arthritis such as rheumatoid arthritis (RA), however, increased osteoclast differentiation and activity skew this balance resulting in progressive bone loss. O-GlcNAcylation is a posttranslational modification with attachment of a single O-linked β-D-N-acetylglucosamine (O-GlcNAc) residue to serine or threonine residues of target proteins. Although O-GlcNAcylation is one of the most common protein modifications, its role in bone homeostasis has not been systematically investigated. We demonstrate that dynamic changes in O-GlcNAcylation are required for osteoclastogenesis. Increased O-GlcNAcylation promotes osteoclast differentiation during the early stages, whereas its downregulation is required for osteoclast maturation. At the molecular level, O-GlcNAcylation affects several pathways including oxidative phosphorylation and cell-cell fusion. TNFα fosters the dynamic regulation of O-GlcNAcylation to promote osteoclastogenesis in inflammatory arthritis. Targeted pharmaceutical or genetic inhibition of O-GlcNAc transferase (OGT) or O-GlcNAcase (OGA) arrests osteoclast differentiation during early stages of differentiation and during later maturation, respectively, and ameliorates bone loss in experimental arthritis. Knockdown of NUP153, an O-GlcNAcylation target, has similar effects as OGT inhibition and inhibits osteoclastogenesis. These findings highlight an important role of O-GlcNAcylation in osteoclastogenesis and may offer the potential to therapeutically interfere with pathologic bone resorption.

Identifiers

PMID35879285
PMCPMC9314416
OpenAlexW4287831838

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.