Evidence map›Paper›PMID 31964464›Full record

ArticleBMB reports2020

Physalin D inhibits RANKL-induced osteoclastogenesis and bone loss via regulating calcium signaling.

Ning Ding, Yanzhu Lu, Hanmin Cui, Qinyu Ma, Dongxia Qiu, Xueting Wei, Ce Dou, Ning Cao

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Comparative Transcriptomics RevealedPlants (Basel, Switzerland) · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Physiologic osteoclasts are not sufficient to induce skeletal pain in mice.European journal of pain (London, England) · 2021
    Article
  9. The Role of CaInternational journal of molecular sciences · 2020
    Review
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

8 authors at 3 institutions in 1 country.

Ning DingDepartment of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China.
Yanzhu LuDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.
Hanmin CuiDepartment of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China.
Qinyu MaDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.
Dongxia QiuDepartment of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China.
Xueting WeiDepartment of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China.
Ce DouDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.
Ning CaoDepartment of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China.
General Hospital of Shenyang Military Region · CNSouthwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the effects of physalin A, B, D, and F on osteoclastogenesis induced by receptor activator of nuclear factor κB ligand (RANKL). The biological functions of different physalins were first predicted using an in silico bioinformatic tool (BATMAN-TCM). Afterwards, we tested cell viability and cell apoptosis rate to analyze the cytotoxicity of different physalins. We analyzed the inhibitory effects of physalins on RANKL-induced osteoclastogenesis from mouse bone-marrow macrophages (BMMs) using a tartrate-resistant acid phosphatase (TRAP) stain. We found that physalin D has the best selectivity index (SI) among all analyzed physalins. We then confirmed the inhibitory effects of physalin D on osteoclast maturation and function by immunostaining of F-actin and a pit-formation assay. On the molecular level, physalin D attenuated RANKLevoked intracellular calcium ([Ca(2+)](i)) oscillation by inhibiting phosphorylation of phospholipase Cγ2 (PLCγ2) and thus blocked the downstream activation of Ca2+/calmodulindependent protein kinases (CaMK)IV and cAMP-responsive element-binding protein (CREB). An animal study showed that physalin D treatment rescues bone microarchitecture, prevents bone loss, and restores bone strength in a model of rapid bone loss induced by soluble RANKL. Taken together, these results suggest that physalin D inhibits RANKL-induced osteoclastogenesis and bone loss via suppressing the PLCγ2-CaMK-CREB pathway. [BMB Reports 2020; 53(3): 154-159].

Indexed as

AnimalsBone and BonesBone Marrow CellsBone ResorptionCalciumCalcium SignalingCell DifferentiationFemaleMacrophagesMiceMice, Inbred C57BLNFATC Transcription FactorsNF-kappa BOsteoclastsOsteogenesisRANK LigandCalciumNFATC Transcription FactorsNF-kappa Bphysalin DRANK LigandSecosteroidsTnfsf11 protein, mouse

Identifiers

PMID31964464
PMCPMC7118355
OpenAlexW3013697842

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.