Evidence map›Paper›PMID 30103522›Full record

ReviewInternational journal of molecular sciences2018

Modulation of Apoptosis by Cytotoxic Mediators and Cell-Survival Molecules in Sjögren's Syndrome.

Hideki Nakamura, Yoshiro Horai, Toshimasa Shimizu, Atsushi Kawakami

Open access · goldAbstract readReview
In one paragraph

Review 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 46 citations in OpenAlex.

  1. FASN-mediated metabolic reprogramming drives CD4Arthritis research & therapy · 2026
    Article
  2. Article
  3. Article
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  5. ACSS2/AATF Drives Soluble FasL-Mediated CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Review
  7. Review
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  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Therapeutic Functions of Stem Cells from Oral Cavity: An Update.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Mechanisms of Disease in Sjögren Syndrome-New Developments and Directions.International journal of molecular sciences · 2020
    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

4 authors at 2 institutions in 1 country.

Hideki NakamuraDepartment of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki City, Nagasaki 852-8501, Japan. nhideki@nagasaki-u.ac.jp.
Yoshiro HoraiClinical Research Center, National Hospital Organization Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8562, Japan. horaiy@nagasaki-mc.com.
Toshimasa ShimizuDepartment of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki City, Nagasaki 852-8501, Japan. toshimasashimizu2000@yahoo.co.jp.
Atsushi KawakamiDepartment of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki City, Nagasaki 852-8501, Japan. atsushik@nagasaki-u.ac.jp.
Nagasaki University · JPNagasaki Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of Sjögren's syndrome (SS) involves multiple factors including genetic background, cell death, and exocrine dysfunction. We here discuss apoptotic control in exocrine glands in SS by showing various pro- and anti-apoptotic pathways. Although the membrane-bound and soluble form of the Fas/Fas ligand system is a leading player with activation of the death domain and caspase 8/3 cleavage, the role of soluble Fas/FasL (including its polymorphism) in apoptosis is controversial. The tumor necrosis factor related apoptosis-inducing ligand (TRAIL)-mediated apoptosis of salivary gland epithelial cells (SGECs) involves a mitochondrial pathway that includes caspase 9 cleavage. The involvement of innate immunity cells such as toll-like receptors (TLRs) has been investigated; TLR2-4 and TLR7-9 are associated with the induction of inflammation in exocrine glands of SS patients. TLR3 has the potential to induce the apoptosis of SS patients' SGECs. Linkage of epidermal growth factor (EGF) was shown in exocrine glands in SS, and it inhibited the Fas/FasL system with the help of cell-survival factors. TLR3 has dual actions to cause inflammation as well as apoptosis, which are inhibited by EGF. In conclusion, apoptosis in exocrine glands of SS patients is tightly controlled by balance of pro-apoptotic signals and growth factor.

Indexed as

ApoptosisAnimalsCaspase 9Cell SurvivalEpidermal Growth FactorExocrine GlandsFas Ligand Proteinfas ReceptorHumansSjogren's SyndromeToll-Like ReceptorsCASP9 protein, humanCaspase 9Epidermal Growth FactorFASLG protein, humanFas Ligand ProteinFAS protein, humanfas ReceptorToll-Like Receptorsapoptosiscell survival moleculeEGFFassalivary gland epithelial cellsSjögren’s syndromeTLR

Identifiers

PMID30103522
PMCPMC6121505
OpenAlexW2887849657

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.