Evidence map›Paper›PMID 32347017›Full record

ArticleJournal of cellular and molecular medicine2020

Triptolide prevents bone loss via suppressing osteoclastogenesis through inhibiting PI3K-AKT-NFATc1 pathway.

Jin Cui, Xiaoqun Li, Sicheng Wang, Yiming Su, Xiao Chen, Liehu Cao, Xin Zhi, Zili Qiu, Yao Wang, Hao Jiang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
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  9. Extract ofCells · 2024
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  13. AS-605240 Blunts Osteoporosis by Inhibition of Bone Resorption.Drug design, development and therapy · 2023
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  14. Review
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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

13 authors at 4 institutions in 2 countries.

Jin CuiDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Xiaoqun LiGraduate Management Unit, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Sicheng WangZhongye Hospital, Shanghai, China.
Yiming SuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Xiao ChenDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Liehu CaoDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Xin ZhiGraduate Management Unit, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Zili QiuJinling High School, Nanjing, China.
Yao WangDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Hao JiangDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Biaotong HuangInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Fang JiDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Jiacan SuDepartment of Orthopedics, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.ORCID 0000-0001-7080-263X
Second Military Medical University · CNShanghai University · CNJinling Institute of Technology · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone loss (osteopenia) is a common complication in human solid tumour. In addition, after surgical treatment of gynaecological tumour, osteoporosis often occurs due to the withdrawal of oestrogen. The major characteristic of osteoporosis is the low bone mass with micro-architectural deteriorated bone tissue. And the main cause is the overactivation of osteoclastogenesis, which is one of the most important therapeutic targets. Inflammation could induce the interaction of RANKL/RANK, which is the promoter of osteoclastogenesis. Triptolide is derived from the traditional Chinese herb lei gong teng, presented multiple biological effects, including anti-cancer, anti-inflammation and immunosuppression. We hypothesized that triptolide could inhibits osteoclastogenesis by suppressing inflammation activation. In this study, we confirmed that triptolide could suppress RANKL-induced osteoclastogenesis in bone marrow mononuclear cells (BMMCs) and RAW264.7 cells and inhibited the osteoclast bone resorption functions. PI3K-AKT-NFATc1 pathway is one of the most important downstream pathways of RANKL-induced osteogenesis. The experiments in vitro indicated that triptolide suppresses the activation of PI3K-AKT-NFATc1 pathway and the target point located at the upstream of AKT because both NFATc1 overexpression and AKT phosphorylation could ameliorate the triptolide suppression effects. The expression of MDM2 was elevated, which demonstrated the MDM-p53-induced cell death might contribute to the osteoclastogenesis suppression. Ovariectomy-induced bone loss and inflammation activation were also found to be ameliorated in the experiments in vivo. In summary, the new effect of anti-cancer drug triptolide was demonstrated to be anti-osteoclastogenesis, and we demonstrated triptolide might be a promising therapy for bone loss caused by tumour.

Indexed as

OsteogenesisSignal TransductionAcetatesAnimalsBenzopyransBiomarkersBone ResorptionDiterpenesEpoxy CompoundsFemaleMiceMice, Inbred C57BLNFATC Transcription FactorsOsteoclastsOvariectomyPhenanthrenesAcetatesAKT activator SC79BenzopyransBiomarkersDiterpenesEpoxy CompoundsNFATC Transcription FactorsPhenanthrenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2RANK Ligandtriptolidebone lossovariectomyPI3K-AKT-NFATc1triptolidetumour

Identifiers

PMID32347017
PMCPMC7294126
OpenAlexW3019004096

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.