Evidence map›Paper›PMID 26275440›Full record

ReviewCurrent diabetes reports2015

The CXCR1/2 Pathway: Involvement in Diabetes Pathophysiology and Potential Target for T1D Interventions.

Antonio Citro, Elisa Cantarelli, Lorenzo Piemonti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Chemokines in Type 1 Diabetes Mellitus.Frontiers in immunology · 2021
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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

3 authors at 2 institutions in 1 country.

Antonio CitroSan Raffaele Diabetes Research Institute, IRCCS San Raffaele Scientific Institute, Milan, Italy, citro.antonio@hsr.it.
Elisa Cantarelli
Lorenzo Piemonti
Vita-Salute San Raffaele University · ITIstituto di Ricovero e Cura a Carattere Scientifico San Raffaele

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although numerous chemokine/chemokine receptor pathways have been described to be implicated in the pathogenesis of type 1 diabetes (T1D), the CXCR1/2 axis has recently been proved to be crucial for leucocyte recruitment involved in insulitis and β cell damage. Multiple strategies blocking the CXCR1/2 pathway are available such as neutralizing antibodies, small molecules and peptide-derived inhibitors. They were firstly and widely used in cancer thanks to their anti-tumorigenic activity and only recently they were tested as a new interventional approach for T1D. As well, CXCR1/2 inhibition has been demonstrated to prevent inflammation- and autoimmunity-mediated damage of the pancreatic islets through inhibiting the migration of CXCR1/2-expressing cells. Among them, neutrophils, macrophages, and, although to a smaller extent, lymphoid cells are the main CXCR1/2-expressing cells. These results supported the active role of the innate immunity in the autoimmune process and opened new interventional approaches for the management of T1D.

Indexed as

Signal TransductionAnimalsDiabetes Mellitus, Type 1HumansIslets of LangerhansNeutrophilsReceptors, Interleukin-8AReceptors, Interleukin-8BReceptors, Interleukin-8AReceptors, Interleukin-8B

Identifiers

PMID26275440
OpenAlexW1164787757

What OpenQuestion holds

Textmetadata
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.