Evidence map›Paper›PMID 26136626›Full record

ReviewMediators of inflammation2015

Cross Talk between Proliferative, Angiogenic, and Cellular Mechanisms Orchestred by HIF-1α in Psoriasis.

Azael Torales-Cardeña, Isaí Martínez-Torres, Sandra Rodríguez-Martínez, Fernando Gómez-Chávez, Juan C Cancino-Díaz, Ernesto A Vázquez-Sánchez, Mario E Cancino-Díaz

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. HIFZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. 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

7 authors at 2 institutions in 1 country.

Azael Torales-CardeñaImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Isaí Martínez-TorresImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Sandra Rodríguez-MartínezImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Fernando Gómez-ChávezImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Juan C Cancino-DíazMicrobiology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Ernesto A Vázquez-SánchezImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Mario E Cancino-DíazImmunology Department, National School of Biological Sciences, National Polytechnic Institute, Plan de Ayala y Prolongación de Carpio S/N, Colonia Santo Tomás, Miguel Hidalgo, 11340 Mexico City, DF, Mexico.
Tecnológico Nacional de México · MXInstituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory skin disease where the altered regulation in angiogenesis, inflammation, and proliferation of keratinocytes are the possible causes of the disease, and the transcription factor "hypoxia-inducible factor 1-alpha" (HIF-1α) is involved in the homeostasis of these three biological phenomena. In this review, the role of HIF-1α in the cross talk between the cytokines and cells of the immunological system involved in the pathogenesis of psoriasis is discussed.

Indexed as

AnimalsCell PolarityCell ProliferationCytokinesDisease Models, AnimalHumansHypoxia-Inducible Factor 1, alpha SubunitInterleukin-1MiceNeovascularization, PhysiologicPsoriasisTh17 CellsVascular Endothelial Growth Factor ACytokinesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInterleukin-1interleukin 36, humanVascular Endothelial Growth Factor A

Identifiers

PMID26136626
PMCPMC4475568
OpenAlexW1585687842

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.