Evidence map›Paper›PMID 41250977›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Identification and Mechanisms of Osteocyte Subsets Involved in the Pathological Progression of Osteoporosis.

Zengxin Jiang, Biyu Rui, Xuecheng He, Jiajun Wang, Xiangdong Wu, Rui Shao, Xue Meng, Xiaochun Peng, Hengfeng Yuan

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

9 authors.

Zengxin JiangDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.
Biyu RuiDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.
Xuecheng HeDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.
Jiajun WangDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.
Xiangdong WuDepartment of Orthopaedics, Beijing Jishuitan Hospital, Capital Medical University, Beijing, 100035, China.
Rui ShaoInstitute of Microsurgery on Extremities, Shanghai JiaoTong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Xue MengInstitute of Microsurgery on Extremities, Shanghai JiaoTong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Xiaochun PengDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.
Hengfeng YuanDepartment of Orthopaedics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai, 200233, China.ORCID https://orcid.org/0000-0003-0017-2622

Funding

National Natural Science Foundation of China 81702133National Natural Science Foundation of China 82372481National Natural Science Foundation of China 82402850National Natural Science Foundation of China 82472441
6 · The paper itself

Abstract

Osteocytes are the most abundant cell type in bone. However, the detailed functions of osteocyte subsets in osteoporosis have remained obscure. In this study, it is aimed to investigate the impact of osteocyte subset heterogeneity on the pathological process of osteoporosis and new potential molecular mechanisms. Six osteocyte subsets are identified in mouse bones by single-cell sequencing. Among them, the epidermal growth factor receptor (Egfr)+ interleukin-1 receptor type I (Il1r1)+ Semaphorin 5a (Sema5a)+osteocyte subpopulation (bone homeostasis regulatory osteocytes, BHR-Ocys) played a key role in the maintenance of bone homeostasis by regulating osteoblasts and osteoclasts. The data confirm that the increased proportion of BHR-Ocys contributes to bone loss in the postmenopausal osteoporotic mice. Mechanistically, Sema5a derived from BHR-Ocys binds to the osteoclast receptor protein Plexin A1 (Plxna1), thereby activating the phosphatidylinositol-3 kinase/protein kinase B/myelocytomatosis oncogen (PI3K/AKT/Myc) signaling pathway, leading to active osteoclast-mediated bone resorption. In conclusion, BHR-Ocys is a key cell subpopulation in the regulation of bone homeostasis. The Sema5a-Plxna1 axis is an important mechanism for BHR-Ocys to regulate osteoclast differentiation. The study provides new insights into the role and mechanism of osteocytes in the regulation of bone homeostasis and identifies new targets for the prevention and treatment of osteoporosis.

Indexed as

OsteocytesOsteoporosisAnimalsDisease Models, AnimalDisease ProgressionFemaleHumansMiceMice, Inbred C57BLOsteoclastsSignal Transductionbone homeostasisosteocyte subsetsosteoporosisSema5a

Identifiers

PMID41250977
PMCPMC12850396

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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.