Evidence map›Paper›PMID 29695130›Full record

ArticleInternational journal of molecular sciences2018

HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloid Development.

Satoko Yamawaki, Motoko Naitoh, Hiroshi Kubota, Rino Aya, Yasuhiro Katayama, Toshihiro Ishiko, Taku Tamura, Katsuhiro Yoshikawa, Tatsuki Enoshiri, Mika Ikeda and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  10. Recent Advances in Scar Biology.International journal of molecular sciences · 2018
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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

11 authors at 6 institutions in 1 country.

Satoko YamawakiDepartment of Plastic and Reconstructive Surgery, Japanese Red Cross Fukui Hospital, 2-4-1, Tsukimi, Fukui-City, Fukui 918-8501, Japan. satokoy@kuhp.kyoto-u.ac.jp.
Motoko NaitohDepartment of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. mnaitoh@kuhp.kyoto-u.ac.jp.
Hiroshi KubotaDepartment of Life Science, Faculty of Engineering Science, Akita University, 1-1 Tegata Gakuenmachi, Akita 010-8502, Japan. hkubota@gipc.akita-u.ac.jp.
Rino AyaDepartment of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. rinok@kuhp.kyoto-u.ac.jp.
Yasuhiro KatayamaDepartment of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. hemim@kuhp.kyoto-u.ac.jp.
Toshihiro IshikoDepartment of Plastic and Reconstructive Surgery, Japanese Red Cross Otsu Hospital, 1-1-35, Nagara, Otsu City, Shiga 520-8511, Japan. ishiko@otsu.jrc.or.jp.
Taku TamuraDepartment of Life Science, Faculty of Engineering Science, Akita University, 1-1 Tegata Gakuenmachi, Akita 010-8502, Japan. taku@gipc.akita-u.ac.jp.ORCID 0000-0001-6074-9273
Katsuhiro YoshikawaDepartment of Plastic and Reconstructive Surgery, Shiga Medical Center for Adults, 5-4-30, Moriyama, Moriyama City, Shiga 524-8524, Japan. khiro@kuhp.kyoto-u.ac.jp.
Tatsuki EnoshiriDepartment of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. enotatsu@kuhp.kyoto-u.ac.jp.
Mika IkedaDepartment of Plastic and Reconstructive Surgery, Kobe City Medical Center General Hospital, 2-1-1, Minatojima minami-machi, Cyuou-ku, Kobe City, Hyogo 650-0047, Japan. mikaring@crux.ocn.ne.jp.
Shigehiko SuzukiDepartment of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. ssuzuk@kuhp.kyoto-u.ac.jp.
Kyoto University · JPAkita University · JPFukui Red Cross Hospital · JPKobe City Medical Center General Hospital · JPOtsu Red Cross Hospital · JPShiga Medical Center for Adults · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloids occur after failure of the wound healing process; inflammation persists, and various treatments are ineffective. Keloid pathogenesis is still unclear. We have previously analysed the gene expression profiles in keloid tissue and found that HtrA1 was markedly up-regulated in the keloid lesions. HtrA1 is a serine protease suggested to play a role in the pathogenesis of various diseases, including age-related macular degeneration and osteoarthritis, by modulating extracellular matrix or cell surface proteins. We analysed HtrA1 localization and its role in keloid pathogenesis. Thirty keloid patients and twelve unrelated patients were enrolled for in situ hybridization, immunohistochemical, western blot, and cell proliferation analyses. Fibroblast-like cells expressed more HtrA1 in active keloid lesions than in surrounding lesions. The proportion of HtrA1-positive cells in keloids was significantly higher than that in normal skin, and HtrA1 protein was up-regulated relative to normal skin. Silencing

Indexed as

Gene Expression RegulationAdolescentAdultAgedAged, 80 and overBiomarkersBiopsyCell ProliferationCells, CulturedFemaleFibroblastsGene Knockdown TechniquesHigh-Temperature Requirement A Serine Peptidase 1HumansImmunohistochemistryKeloidBiomarkersHigh-Temperature Requirement A Serine Peptidase 1HTRA1 protein, humanRNA, Messengerfibroproliferative disorderHtrA1inflammationkeloids

Identifiers

PMID29695130
PMCPMC5983720
OpenAlexW2765735926

What OpenQuestion holds

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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.