Evidence map›Paper›PMID 27031959›Full record

ArticleCell death & disease2016

Dihydroartemisinin attenuates lipopolysaccharide-induced osteoclastogenesis and bone loss via the mitochondria-dependent apoptosis pathway.

C Dou, N Ding, J Xing, C Zhao, F Kang, T Hou, H Quan, Y Chen, Q Dai, F Luo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.1field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Pooled it
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  3. Review
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  11. Frontiers in immunology · 2022
    Article
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  14. Review
  15. Article
  16. Article
  17. Iron Promotes Dihydroartemisinin CytotoxicityFrontiers in pharmacology · 2020
    Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

C DouDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
N DingDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
J XingDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
C ZhaoDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing 400038, China.
F KangDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing 400038, China.
T HouDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
H QuanDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing 400038, China.
Y ChenDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing 400038, China.
Q DaiDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
F LuoDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
J XuDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
S DongDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing 400038, China.
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dihydroartemisinin (DHA) is a widely used antimalarial drug isolated from the plant Artemisia annua. Recent studies suggested that DHA has antitumor effects utilizing its reactive oxygen species (ROS) yielding mechanism. Here, we reported that DHA is inhibitory on lipopolysaccharide (LPS)-induced osteoclast (OC) differentiation, fusion and bone-resorption activity in vitro. Intracellular ROS detection revealed that DHA could remarkably increase ROS accumulation during LPS-induced osteoclastogenesis. Moreover, cell apoptosis was also increased by DHA treatment. We found that DHA-activated caspase-3 increased Bax/Bcl-2 ratio during LPS-induced osteoclastogenesis. Meanwhile, the translocation of apoptotic inducing factor (AIF) and the release of cytochrome c from the mitochondria into the cytosol were observed, indicating that ROS-mediated mitochondrial dysfunction is crucial in DHA-induced apoptosis during LPS-induced osteoclastogenesis. In vivo study showed that DHA treatment decreased OC number, prevents bone loss, rescues bone microarchitecture and restores bone strength in LPS-induced bone-loss mouse model. Together, our findings indicate that DHA is protective against LPS-induced bone loss through apoptosis induction of osteoclasts via ROS accumulation and the mitochondria-dependent apoptosis pathway. Therefore, DHA may be considered as a new therapeutic candidate for treating inflammatory bone loss.

Indexed as

Actin CytoskeletonAnimalsAntimalarialsApoptosisArtemisia annuaArtemisininsBone and BonesCaspase 3Cell DifferentiationCell LineFemaleLipopolysaccharidesMatrix Metalloproteinase 9MiceMice, Inbred C57BLMitochondriaAcp5 protein, mouseAntimalarialsArtemisininsartenimolCaspase 3LipopolysaccharidesMatrix Metalloproteinase 9Mmp9 protein, mouseReactive Oxygen SpeciesTartrate-Resistant Acid Phosphatase

Identifiers

PMID27031959
PMCPMC4823966
OpenAlexW2321061041

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.