Evidence map›Paper›PMID 33800389›Full record

ReviewInternational journal of molecular sciences2021

Isoform-Selective NFAT Inhibitor: Potential Usefulness and Development.

Noriko Kitamura, Osamu Kaminuma

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. NFATC3 enhances osteosarcoma progression by increasing PD-L1 and CXCL2 levels.Medical oncology (Northwood, London, England) · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. NOD1: a metabolic modulator.Frontiers in endocrinology · 2024
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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

2 authors at 2 institutions in 1 country.

Noriko KitamuraLaboratory of Allergy and Immunology, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Osamu KaminumaLaboratory of Allergy and Immunology, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.ORCID 0000-0003-1211-0410
Hiroshima University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

Japan Society for the Promotion of Science 21590086Japan Society for the Promotion of Science 24590107Terumo Foundation for Life Sciences and Arts
6 · The paper itself

Abstract

Nuclear factor of activated T cells (NFAT), which is the pharmacological target of immunosuppressants cyclosporine and tacrolimus, has been shown to play an important role not only in T cells (immune system), from which their name is derived, but also in many biological events. Therefore, functional and/or structural abnormalities of NFAT are linked to the pathogenesis of diseases in various organs. The NFAT protein family consists of five isoforms, and each isoform performs diverse functions and has unique expression patterns in the target tissues. This diversity has made it difficult to obtain ideal pharmacological output for immunosuppressants that inhibit the activity of almost all NFAT family members, causing serious and wide-ranging side effects. Moreover, it remains unclear whether isoform-selective NFAT regulation can be achieved by targeting the structural differences among NFAT isoforms and whether this strategy can lead to the development of better drugs than the existing ones. This review summarizes the role of the NFAT family members in biological events, including the development of various diseases, as well as the usefulness of and problems associated with NFAT-targeting therapies, including those dependent on current immunosuppressants. Finally, we propose a novel therapeutic strategy based on the molecular mechanisms that enable selective regulation of specific NFAT isoforms.

Indexed as

AnimalsCyclosporineHumansImmunosuppressive AgentsNFATC Transcription FactorsProtein IsoformsTacrolimusT-LymphocytesCyclosporineImmunosuppressive AgentsNFATC Transcription FactorsProtein IsoformsTacrolimusaortic smooth muscle cellcalcineurin-binding regioncytokineimmunoprecipitationimmunosuppressantknockout mousemolecular operating environmentnuclear localization signal

Identifiers

PMID33800389
PMCPMC7962815
OpenAlexW3133761729

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.