Evidence map›Paper›PMID 28387719›Full record

ReviewInternational journal of molecular sciences2017

Emerging Roles of IL-33/ST2 Axis in Renal Diseases.

Wei-Yu Chen, Lung-Chih Li, Jenq-Lin Yang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. ST2 Signaling Regulates Innate Immune Responses in Kidney Injury.bioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. ST2 + T-Regulatory Cells in Renal Inflammation and Fibrosis after Ischemic Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Soluble suppression of tumorigenicity-2 in pregnancy with a small-for-gestational-age fetus and with preeclampsia.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021
    Review
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Wei-Yu ChenInstitute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. wychen624@cgmh.org.tw.
Lung-Chih LiInstitute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. r5239@cgmh.org.tw.
Jenq-Lin YangInstitute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. jyang@adm.cgmh.org.tw.
Kaohsiung Chang Gung Memorial Hospital · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), have a great impact on health care systems worldwide. Similar to cardiovascular diseases, renal diseases are inflammatory diseases involving a variety of cytokines. Primary causes of renal injury include ischemia, uremic toxins, bacteremia, or nephrotoxicity. Inflammation represents an important component following kidney injury. Interleukin (IL)-33 is a member of the IL-1 cytokine family, which is widely expressed in epithelial barrier tissues and endothelial cells, and mediates both tissue inflammation and repair responses. IL-33 is released as a nuclear alarmin in response to tissue damage and triggers innate and adaptive immune responses by binding to its receptor, suppression of tumorigenicity 2 (ST2). Recent evidence from clinical and experimental animal studies indicates that the IL-33/ST2 axis is involved in the pathogenesis of CKD, renal graft injury, systemic lupus nephritis, and AKI. In this review, we discuss the pathological and tissue reparative roles of the IL-33/ST2 pathway in different types of renal diseases.

Indexed as

Adaptive ImmunityAnimalsCell NucleusHumansImmunity, InnateInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Kidney DiseasesSignal TransductionIL1RL1 protein, humanIL33 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33acute renal injurychronic renal diseaseinflammationinterleukin-33

Identifiers

PMID28387719
PMCPMC5412367
OpenAlexW2604256973

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.