Evidence map›Paper›PMID 32443893›Full record

ArticleInternational journal of molecular sciences2020

Inflammatory Skin-Derived Cytokines Accelerate Osteoporosis in Mice with Persistent Skin Inflammation.

Kento Mizutani, Kana Isono, Yoshiaki Matsushima, Karin Okada, Ai Umaoka, Shohei Iida, Koji Habe, Kohei Hagimori, Hidetoshi Yamazaki, Keiichi Yamanaka

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  15. Special Issue: "Skin Disease and Comorbidities".Journal of clinical medicine · 2021
    Article
  16. Osteoporosis in Skin Diseases.International journal of molecular sciences · 2020
    Review
  17. 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

10 authors at 2 institutions in 1 country.

Kento MizutaniDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Kana IsonoStem Cell and Developmental Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Yoshiaki MatsushimaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Karin OkadaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Ai UmaokaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Shohei IidaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Koji HabeDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Kohei HagimoriMedicines Development Unit Japan, Eli Lilly Japan K.K., 5-1-28 Isogamidori, Chuo-ku, Kobe, Hyogo 651-0086, Japan.
Hidetoshi YamazakiStem Cell and Developmental Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Keiichi YamanakaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Mie University · JPEli Lilly (Japan) · JP

Funding

AbbVie GK nonEli Lilly and Company non
6 · The paper itself

Abstract

Secondary osteoporosis can also be caused by chronic inflammatory skin disease as well as rheumatoid arthritis or inflammatory bowel disease. However, the exact role of osteoporosis in inflammatory skin conditions has not been elucidated. Using a mouse model of dermatitis, we investigated the pathophysiology of osteoporosis in inflammatory skin conditions and the therapeutic impact of osteoporosis medication on inflammatory skin disease. We employed model mice of spontaneous skin inflammation, specifically overexpressing human caspase-1 in the epidermis. Bone density and the expression of various mRNAs in the femur were examined by micro CT and RT-PCR. The effects of minodronate and anti-RANKL antibody on bone structure, histology, and femur blood flow were studied. The mouse model of skin inflammation showed a marked decrease in bone density compared to wild-type littermates with abnormalities in both bone resorption and formation. Minodronate improved bone density by decreasing osteoclasts, but anti-RANKL antibody did not improve. In the dermatitis model, the blood flow in the bone marrow was decreased, and minodronate restored this parameter. A model of persistent dermatitis exhibited marked osteoporosis, but the impact of chronic dermatitis on osteoporosis has not been thoroughly investigated. We should explore the pathogenesis of osteoporosis in skin inflammatory diseases.

Indexed as

AnimalsBone DensityBone Density Conservation AgentsBone RemodelingCaspase 1CytokinesDiphosphonatesFemaleFemurImidazolesMiceMice, Inbred C57BLOsteoporosisPsoriasisRegional Blood FlowBone Density Conservation AgentsCaspase 1CytokinesDiphosphonatesImidazolesYM 529anti-RANKL antibodyinflammatory skin mouse modelminodronateosteoporosispsoriasis

Identifiers

PMID32443893
PMCPMC7279417
OpenAlexW3027921277

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.