Evidence map›Paper›PMID 30374519›Full record

ArticleCellular and molecular life sciences : CMLS2019

Chemokine-like receptor 1 deficiency leads to lower bone mass in male mice.

Huashan Zhao, Dewen Yan, Liang Xiang, Chen Huang, Jian Li, Xiangfang Yu, Binbin Huang, Baobei Wang, Jie Chen, Tianxia Xiao and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Adipokines: New Therapeutic Target for Osteoarthritis?Current rheumatology reports · 2019
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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

12 authors at 3 institutions in 1 country.

Huashan ZhaoLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Dewen YanDepartment of Endocrinology, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518035, China.
Liang XiangLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Chen HuangLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Jian LiCenter for Translational Medicine Research and Development, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Xiangfang YuCenter for Translational Medicine Research and Development, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Binbin HuangLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Baobei WangLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Jie ChenLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Tianxia XiaoLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Pei-Gen RenDepartment of Endocrinology, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518035, China. pg.ren@siat.ac.cn.
Jian V ZhangLaboratory for Reproductive Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China. jian.zhang@siat.ac.cn.
Shenzhen Institutes of Advanced Technology · CNChinese Academy of Sciences · CNShenzhen University · CN

Funding

National Natural Science Foundation of China 31671562National Natural Science Foundation of China 81771611Natural Science Foundation of Guangdong Province (CN) 2017A020211033Science and Technology Innovation Fund of Shenzhen JCYJ20170307165601938Science and Technology Innovation Fund of Shenzhen JCYJ20170412140326739Science and Technology Innovation Fund of Shenzhen JCYJ20170413165233512Science and Technology Innovation Fund of Shenzhen JCYJ20170413165503382Science and Technology Innovation Fund of Shenzhen JCYJ20170814175916411Science and Technology Innovation Fund of Shenzhen JCYJ20170815123502541
6 · The paper itself

Abstract

The adipokine Chemerin and its receptor, chemokine-like receptor 1 (CMKLR1), are associated with osteoblastogenic differentiation of mesenchymal stem cells (MSCs) and osteoclastogenic differentiation of osteoclast precursors in vitro, suggesting that CMKLR1 would affect the bone mineral density (BMD). However, the role of CMKLR1 on BMD in vivo remains unknown. Here, using CMKLR1 knockout mouse model, we unveiled that CMKLR1 effected the amount of Leydig cells in testis and regulated androgen-dependent bone maintenance in male mice, which exhibited lower serum testosterone levels, thereby reducing the trabecular bone mass. Correspondingly, the mRNA expression of testosterone synthesis enzymes in testis decreased. The bone tissue also showed decreased mRNAs expression of osteogenic markers and increased mRNA levels for osteoclast markers. Furthermore, by in vitro differentiation models, we found CMKLR1-deficiency could break the balance between osteoblastogenesis and osteoclastogenesis that caused a shift from osteogenic to adipogenic differentiation in MSCs and enhanced osteoclast formation. In addition, bone mass increase in CMKLR1 KO male mice can be promoted by treatment with 5α-dihydrotestosterone (DHT), and the inactivation of CMKLR1 in male wild-type (WT) mice with antagonist treatment can lead to low bone mass. Taken together, these data indicate that CMKLR1 positively regulates bone metabolism through mediating testosterone production and the balance between osteoblast and osteoclast formation.

Indexed as

Bone Density3-Hydroxysteroid DehydrogenasesAnimalsCell DifferentiationFatty Acid-Binding ProteinsFemurInterleukin-1betaInterleukin-6Leydig CellsMaleMiceMice, Inbred C57BLMice, KnockoutOsteoclastsOsteogenesisPPAR gamma3-Hydroxysteroid DehydrogenasesCMKLR1 protein, mouseFabp4 protein, mouseFatty Acid-Binding ProteinsInterleukin-1betaInterleukin-6PPAR gammaReceptors, ChemokineReceptors, G-Protein-CoupledTestosteroneAdipokineChemerinCMKLR1OsteoporosisTestosterone

Identifiers

PMID30374519
PMCPMC11105338
OpenAlexW2898717912

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.