Evidence map›Paper›PMID 36010655›Full record

ArticleCells2022

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip.

Lijun Zhang, Liqun Xu, Xiaoyan Zhang, Ke Wang, Yingjun Tan, Gaozhi Li, Yixuan Wang, Tong Xue, Quan Sun, Xinsheng Cao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Lijun ZhangThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Liqun XuThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Xiaoyan ZhangThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Ke WangThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Yingjun TanState Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing 100094, China.
Gaozhi LiThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Yixuan WangThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Tong XueThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Quan SunThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Xinsheng CaoThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Ge ZhangInstitute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong 999077, China.ORCID 0000-0002-7807-7695
Zebing HuThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Shu ZhangThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Fei ShiThe Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an 710032, China.
Air Force Medical University · CNChina Astronaut Research and Training Center · CNHong Kong Baptist University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone loss caused by mechanical unloading is a threat to prolonged space flight and human health. Epigenetic modifications play a crucial role in varied biological processes, but the mechanism of histone modification on unloading-induced bone loss has rarely been studied. Here, we discovered for the first time that the methyltransferase Setdb1 was downregulated under the mechanical unloading both in vitro and in vivo so as to attenuate osteoblast proliferation. Furthermore, we found these interesting processes depended on the repression of Macrod2 expression triggered by Setdb1 catalyzing the formation of H3K9me3 in the promoter region. Mechanically, we revealed that Macrod2 was upregulated under mechanical unloading and suppressed osteoblast proliferation through the GSK-3β/β-catenin signaling pathway. Moreover, Atf7ip cooperatively contributed to osteoblast proliferation by changing the localization of Setdb1 under mechanical loading. In summary, this research elucidated the role of the Atf7ip/Setdb1/Macrod2 axis in osteoblast proliferation under mechanical unloading for the first time, which can be a potential protective strategy against unloading-induced bone loss.

Indexed as

Biological PhenomenaEpigenesis, GeneticCell ProliferationDNA Repair EnzymesGlycogen Synthase Kinase 3 betaHistone-Lysine N-MethyltransferaseHumansHydrolasesOsteoblastsRepressor ProteinsATF7IP protein, humanDNA Repair EnzymesGlycogen Synthase Kinase 3 betaHistone-Lysine N-MethyltransferaseHydrolasesMACROD2 protein, humanRepressor ProteinsSETDB1 protein, humanbone losscell proliferationmechanical unloadingSetdb1

Identifiers

PMID36010655
PMCPMC9406310
OpenAlexW4292549039

What OpenQuestion 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 OpenQuestion graph.