Evidence map›Paper›PMID 34502368›Full record

ReviewInternational journal of molecular sciences2021

Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.

Davide Ferrari, Fabio Casciano, Paola Secchiero, Eva Reali

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. 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
3.6field-weighted citation impact, top 8% 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, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Clodronate: The Influence on ATP Purinergic Signaling.Current rheumatology reviews · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Macrophage P2YActa pharmaceutica Sinica. B · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. From the Skin to Distant Sites: T Cells in Psoriatic Disease.International journal of molecular sciences · 2023
    Review
  14. The P2X7 Receptor in Autoimmunity.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Davide FerrariDepartment of Life Science and Biotechnology, Section of Microbiology and Applied Pathology, University of Ferrara, 44121 Ferrara, Italy.
Fabio CascianoDepartment of Translational Medicine and LTTA Centre, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0002-6431-3335
Paola SecchieroDepartment of Translational Medicine and LTTA Centre, University of Ferrara, 44121 Ferrara, Italy.
Eva RealiDepartment of Biotechnology and Biosciences, University of Milano-Bicocca, 20126 Milan, Italy.ORCID 0000-0003-1900-1356
University of Ferrara · ITUniversity of Milano-Bicocca · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory disease of the skin associated with systemic and joint manifestations and accompanied by comorbidities, such as metabolic syndrome and increased risk of cardiovascular disease. Psoriasis has a strong genetic basis, but exacerbation requires additional signals that are still largely unknown. The clinical manifestations involve the interplay between dendritic and T cells in the dermis to generate a self-sustaining inflammatory loop around the TNFα/IL-23/IL-17 axis that forms the psoriatic plaque. In addition, in recent years, a critical role of keratinocytes in establishing the interplay that leads to psoriatic plaques' formation has re-emerged. In this review, we analyze the most recent evidence of the role of keratinocytes and danger associates molecular patterns, such as extracellular ATP in the generation of psoriatic skin lesions. Particular attention will be given to purinergic signaling in inflammasome activation and in the initiation of psoriasis. In this phase, keratinocytes' inflammasome may trigger early inflammatory pathways involving IL-1β production, to elicit the subsequent cascade of events that leads to dendritic and T cell activation. Since psoriasis is likely triggered by skin-damaging events and trauma, we can envisage that intracellular ATP, released by damaged cells, may play a role in triggering the inflammatory response underlying the pathogenesis of the disease by activating the inflammasome. Therefore, purinergic signaling in the skin could represent a new and early step of psoriasis; thus, opening the possibility to target single molecular actors of the purinome to develop new psoriasis treatments.

Indexed as

HumansInflammasomesInflammationInterleukin-17Interleukin-1betaInterleukin-23KeratinocytesPsoriasisPurinesReceptors, Purinergic P1Receptors, Purinergic P2Signal TransductionSkinTumor Necrosis Factor-alphaInflammasomesInterleukin-17Interleukin-1betaInterleukin-23PurinesReceptors, Purinergic P1Receptors, Purinergic P2Tumor Necrosis Factor-alphaenvironmental triggerinflammasome activationP1 receptorsP2 receptorspsoriasis initiationpsoriasis pathogenesispurinergic signaling

Identifiers

PMID34502368
PMCPMC8430580
OpenAlexW3197589315

What Socratic 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 Socratic graph.