Evidence map›Paper›PMID 35256591›Full record

ArticleBone research2022

mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel Scn1a.

Ajuan Chen, Jian Jin, Shasha Cheng, Zezheng Liu, Cheng Yang, Qingjing Chen, Wenquan Liang, Kai Li, Dawei Kang, Zhicong Ouyang and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  6. Osteoblast-CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  8. Review
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  15. International journal of molecular sciences · 2023
    Article
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  18. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Ajuan Chen *Academy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Jian Jin *Department of Spine Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shasha ChengDepartment of Clinical Laboratory, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Zezheng LiuAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Cheng YangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Qingjing ChenAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Wenquan LiangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0003-0881-6808
Kai LiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Dawei KangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Zhicong OuyangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Chenfeng YaoAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Xiaochun BaiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0001-9631-4781
Qingchu LiAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Dadi JinAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China. nyorthop@163.com.
Bin HuangAcademy of Orthopedics, Guangdong Province, Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Spine Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China. binxue483@163.com.ORCID http://orcid.org/0000-0001-6295-6647
Third Affiliated Hospital of Southern Medical University · CNNanfang Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172507Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2018A030313937Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2019A1515011876
6 · The paper itself

Abstract

Senescence impairs preosteoblast expansion and differentiation into functional osteoblasts, blunts their responses to bone formation-stimulating factors and stimulates their secretion of osteoclast-activating factors. Due to these adverse effects, preosteoblast senescence is a crucial target for the treatment of age-related bone loss; however, the underlying mechanism remains unclear. We found that mTORC1 accelerated preosteoblast senescence in vitro and in a mouse model. Mechanistically, mTORC1 induced a change in the membrane potential from polarization to depolarization, thus promoting cell senescence by increasing Ca

Identifiers

PMID35256591
PMCPMC8901653
OpenAlexW4220672052

What OpenQuestion holds

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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.