Evidence map›Paper›PMID 28937683›Full record

ArticleCell death and differentiation2018

A vitronectin-derived peptide reverses ovariectomy-induced bone loss via regulation of osteoblast and osteoclast differentiation.

Seung-Ki Min, Hyun Ki Kang, Sung Youn Jung, Da Hyun Jang, Byung-Moo Min

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  6. Potential Targeting Mechanisms for Bone-Directed Therapies.International journal of molecular sciences · 2024
    Review
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  16. Characterization of Extracellular Vesicles in Osteoporotic Patients Compared to Osteopenic and Healthy Controls.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
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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

5 authors at 2 institutions in 1 country.

Seung-Ki MinOral Oncology Clinic, Research Institute and Hospital, National Cancer Center, Goyang-Si, Gyeonggi-Do 10408, Republic of Korea.
Hyun Ki KangDepartment of Oral Biochemistry and Program in Cancer and Developmental Biology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea.
Sung Youn JungDepartment of Oral Biochemistry and Program in Cancer and Developmental Biology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea.
Da Hyun JangDepartment of Oral Biochemistry and Program in Cancer and Developmental Biology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea.
Byung-Moo MinDepartment of Oral Biochemistry and Program in Cancer and Developmental Biology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea.
Seoul National University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis affects millions of people worldwide by promoting bone resorption and impairing bone formation. Bisphosphonates, commonly used agents to treat osteoporosis, cannot reverse the substantial bone loss that has already occurred by the time of diagnosis. Moreover, their undesirable side-effects, including osteonecrosis of the jaw, have been reported. Here, we demonstrated that a new bioactive core vitronectin-derived peptide (VnP-16) promoted bone formation by accelerating osteoblast differentiation and activity through direct interaction with β1 integrin followed by FAK activation. Concomitantly, VnP-16 inhibited bone resorption by restraining JNK-c-Fos-NFATc1-induced osteoclast differentiation and αvβ3 integrin-c-Src-PYK2-mediated resorptive function. Moreover, VnP-16 decreased the bone resorbing activity of pre-existing mature osteoclasts without changing their survival rate. Furthermore, VnP-16 had a strong anabolic effect on bone regeneration by stimulating osteoblast differentiation and increasing osteoblast number, and significantly alleviated proinflammatory cytokine-induced bone resorption by restraining osteoclast differentiation and function in murine models. Moreover, VnP-16 could reverse ovariectomy-induced bone loss by both inhibiting bone resorption and promoting bone formation. Given its dual role in promoting bone formation and inhibiting bone resorption, our results suggest that VnP-16 could be an attractive therapeutic agent for treating osteoporosis.

Indexed as

OvariectomyAnimalsBone RegenerationBone ResorptionCell DifferentiationCell LineHumansMaleMiceMice, Inbred C57BLOsteoblastsPeptidesVitronectinPeptidesVitronectin

Identifiers

PMID28937683
PMCPMC5762842
OpenAlexW2758856411

What OpenQuestion holds

Textmetadata
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.