Evidence map›Paper›PMID 38877020›Full record

ArticleNature communications2024

Mitochondria from osteolineage cells regulate myeloid cell-mediated bone resorption.

Peng Ding, Chuan Gao, Jian Zhou, Jialun Mei, Gan Li, Delin Liu, Hao Li, Peng Liao, Meng Yao, Bingqi Wang and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
–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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  4. Bone organoids and mitochondrial reprogramming.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

19 authors.

Peng Ding *Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.ORCID http://orcid.org/0000-0002-9348-8134
Chuan Gao *Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Jian Zhou *Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Jialun Mei *Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Gan LiDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Delin LiuDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.ORCID http://orcid.org/0009-0006-6239-1950
Hao LiDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Peng LiaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.ORCID http://orcid.org/0000-0002-4583-5285
Meng YaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Bingqi WangDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Yafei LuDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Xiaoyuan PengDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.ORCID http://orcid.org/0000-0003-2302-362X
Chenyi JiangDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Jimin YinDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Yigang HuangDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China.
Minghao ZhengCentre for Orthopaedic Translational Research, Medical School, University of Western Australia, Nedlands, WA, 6009, Australia.ORCID http://orcid.org/0000-0003-1185-4768
Youshui GaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China. gaoyoushui@sjtu.edu.cn.ORCID http://orcid.org/0000-0001-9242-2486
Changqing ZhangDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China. zhangcq@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-7408-4126
Junjie GaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 200233, Shanghai, China. colingjj@163.com.ORCID http://orcid.org/0000-0003-4820-8524

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81820108020National Natural Science Foundation of China (National Science Foundation of China) 82072417
6 · The paper itself

Abstract

Interactions between osteolineage cells and myeloid cells play important roles in maintaining skeletal homeostasis. Herein, we find that osteolineage cells transfer mitochondria to myeloid cells. Impairment of the transfer of mitochondria by deleting MIRO1 in osteolineage cells leads to increased myeloid cell commitment toward osteoclastic lineage cells and promotes bone resorption. In detail, impaired mitochondrial transfer from osteolineage cells alters glutathione metabolism and protects osteoclastic lineage cells from ferroptosis, thus promoting osteoclast activities. Furthermore, mitochondrial transfer from osteolineage cells to myeloid cells is involved in the regulation of glucocorticoid-induced osteoporosis, and glutathione depletion alleviates the progression of glucocorticoid-induced osteoporosis. These findings reveal an unappreciated mechanism underlying the interaction between osteolineage cells and myeloid cells to regulate skeletal metabolic homeostasis and provide insights into glucocorticoid-induced osteoporosis progression.

Indexed as

Bone ResorptionFerroptosisMitochondriaMyeloid CellsOsteoclastsOsteoporosisAnimalsCell DifferentiationGlucocorticoidsGlutathioneHumansMaleMiceMice, Inbred C57BLMice, KnockoutGlucocorticoidsGlutathione

Identifiers

PMID38877020
PMCPMC11178781

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.