Evidence map›Paper›PMID 26199463›Full record

ReviewMediators of inflammation2015

Fibrosis Related Inflammatory Mediators: Role of the IL-10 Cytokine Family.

Erna Sziksz, Domonkos Pap, Rita Lippai, Nóra Judit Béres, Andrea Fekete, Attila J Szabó, Ádám Vannay

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
15.1field-weighted citation impact, top 1% 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

152 citing papers in PubMed, 268 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  13. Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

92 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Erna SzikszMTA-SE, Pediatrics and Nephrology Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary ; 1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Domonkos Pap1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Rita Lippai1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Nóra Judit Béres1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Andrea FeketeMTA-SE, Lendület Diabetes Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Attila J SzabóMTA-SE, Pediatrics and Nephrology Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary ; 1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Ádám VannayMTA-SE, Pediatrics and Nephrology Research Group, Bokay Janos Street 53-54, Budapest 1083, Hungary ; 1st Department of Pediatrics, Semmelweis University, Bokay Janos Street 53-54, Budapest 1083, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Importance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney diseases, inflammatory bowel disease, and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem. According to some estimates about 45% of all deaths are attributed to FDs in the developed world. Independently of their etiology the common hallmark of FDs is chronic inflammation. Infiltrating immune cells, endothelial, epithelial, and other resident cells of the injured organ release an orchestra of inflammatory mediators, which stimulate the proliferation and excessive extracellular matrix (ECM) production of myofibroblasts, the effector cells of organ fibrosis. Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function. Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis. Therefore, there is an urgent need for the more comprehensive understanding of the pathomechanism of fibrosis and development of novel diagnostic and therapeutic strategies. In the present review we provide an overview of the common key mediators of organ fibrosis highlighting the role of interleukin-10 (IL-10) cytokine family members (IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26), which recently came into focus as tissue remodeling-related inflammatory cytokines.

Indexed as

CytokinesFibrosisHumansInflammationInterleukin-10CytokinesIL10 protein, humanInterleukin-10

Identifiers

PMID26199463
PMCPMC4495231
OpenAlexW1547680175

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.