Evidence map›Paper›PMID 36610396›Full record

ArticleCell reports2023

Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway.

Satoshi Nunomura, Daisuke Uta, Isao Kitajima, Yasuhiro Nanri, Kosuke Matsuda, Naoko Ejiri, Midori Kitajima, Hitoshi Ikemitsu, Misaki Koga, Sayaka Yamamoto and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
  2. Article
  3. Article
  4. The Past, the Present, and the Future of Periostin in Allergy.Allergy, asthma & immunology research · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Guided monocyte fate to FRβ/CD163Cellular and molecular life sciences : CMLS · 2024
    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

15 authors at 5 institutions in 2 countries.

Satoshi NunomuraDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan. Electronic address: nunomura@cc.saga-u.ac.jp.
Daisuke UtaDepartment of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.
Isao KitajimaDepartment of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.
Yasuhiro NanriDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Kosuke MatsudaDepartment of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.
Naoko EjiriDepartment of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.
Midori KitajimaDepartment of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.
Hitoshi IkemitsuDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Misaki KogaDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Sayaka YamamotoDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Yuko HondaDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Hironobu TakedomiDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.
Tsugunobu AndohDepartment of Pharmacology and Pathophysiology, College of Pharmacy, Kinjo Gakuin University, Nagoya 463-8521, Japan.
Simon J ConwayHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
Kenji IzuharaDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan. Electronic address: kizuhara@cc.saga-u.ac.jp.
Saga Medical School Hospital · JPUniversity of Toyama · JPSaga University · JPIndiana University School of MedicineKinjo Gakuin University · JP

Funding

NEURAL-CREST RELATED HEART DEFECTSR01HL060714 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CONWAY, SIMON JAMES · 1998 to 2017
$4.7M
Cardioprotection and uncoupling myofibroblast-myocyte communicationsR01HL148165 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CONWAY, SIMON JAMES, RUBART-VAN DER LOHE, MICHAEL · 2019 to 2022
$1.6M
NHLBI NIH HHS R01 HL060714NHLBI NIH HHS R01 HL148165
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic relapsing skin disease accompanied by recurrent itching. Although type 2 inflammation is dominant in allergic skin inflammation, it is not fully understood how non-type 2 inflammation co-exists with type 2 inflammation or how type 2 inflammation causes itching. We have recently established the FADS mouse, a mouse model of AD. In FADS mice, either genetic disruption or pharmacological inhibition of periostin, a downstream molecule of type 2 inflammation, inhibits NF-κB activation in keratinocytes, leading to downregulating eczema, epidermal hyperplasia, and infiltration of neutrophils, without regulating the enhanced type 2 inflammation. Moreover, inhibition of periostin blocks spontaneous firing of superficial dorsal horn neurons followed by a decrease in scratching behaviors due to itching. Taken together, periostin links NF-κB-mediated inflammation with type 2 inflammation and promotes itching in allergic skin inflammation, suggesting that periostin is a promising therapeutic target for AD.

Indexed as

Dermatitis, AtopicSkinAnimalsInflammationKeratinocytesMiceNF-kappa BPruritusNF-kappa Batopic dermatitisCP: Immunologyintegrinitchingneutrophilperiostin

Identifiers

PMID36610396
PMCPMC11486451
OpenAlexW4313650204

What OpenQuestion holds

Textmetadata
LicenceTDM
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.