Evidence map›Paper›PMID 35068044›Full record

ArticleEMBO reports2022

Myeloid-derived growth factor (MYDGF) protects bone mass through inhibiting osteoclastogenesis and promoting osteoblast differentiation.

Xiaoli Xu, Yixiang Li, Lingfeng Shi, Kaiyue He, Ying Sun, Yan Ding, Biying Meng, Jiajia Zhang, Lin Xiang, Jing Dong and 4 more

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Xiaoli XuDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Yixiang LiDepartment of Hematology and Medical Oncology, School of Medicine, Emory University, Atlanta, GA, USA.
Lingfeng ShiDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Kaiyue HeDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Ying SunDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Yan DingDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Biying MengDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Jiajia ZhangDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Lin XiangDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Jing DongDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Min LiuDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.
Junxia ZhangDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.ORCID 0000-0003-1350-9001
Lingwei XiangCenters for Surgery and Public Health, Brigham and Women's Hospital, Boston, MA, USA.ORCID 0000-0002-0361-103X
Guangda XiangDepartment of Endocrinology, General Hospital of Central Theater Command, Wuhan, China.ORCID 0000-0002-6044-2308
Central Hospital of Wuhan · CNBrigham and Women's Hospital · USEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whether bone marrow regulates bone metabolism through endocrine and paracrine mechanism remains largely unknown. Here, we found that (i) myeloid cell-specific myeloid-derived growth factor (MYDGF) deficiency decreased bone mass and bone strength in young and aged mice; (ii) myeloid cell-specific MYDGF restoration prevented decreases in bone mass and bone strength in MYDGF knockout mice; moreover, myeloid cell-derived MYDGF improved the progress of bone defects healing, prevented ovariectomy (OVX)-induced bone loss and age-related osteoporosis; (iii) MYDGF inhibited osteoclastogenesis and promoted osteoblast differentiation in vivo and in vitro; and (iv) PKCβ-NF-κB and MAPK1/3-STAT3 pathways were involved in the regulation of MYDGF on bone metabolism. Thus, we concluded that myeloid cell-derived MYDGF is a positive regulator of bone homeostasis by inhibiting bone resorption and promoting bone formation. MYDGF may become a potential novel therapeutic drug for osteoporosis, and bone marrow may become a potential therapeutic target for bone metabolic disorders.

Indexed as

Bone ResorptionInterleukinsOsteogenesisAnimalsBone and BonesCell DifferentiationFemaleIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLNF-kappa BOsteoblastsIntercellular Signaling Peptides and ProteinsInterleukinsMydgf protein, mouseNF-kappa Bbone marrow-derived monocytes and macrophagesmyeloid-derived growth factorosteoblastosteoclastosteoporosis

Identifiers

PMID35068044
PMCPMC8892248
OpenAlexW4206958672

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.