Evidence map›Paper›PMID 38303723›Full record

ArticleiScience2024

Dynamic Boolean modeling of molecular and cellular interactions in psoriasis predicts drug target candidates.

Eirini Tsirvouli, Vincent Noël, Åsmund Flobak, Laurence Calzone, Martin Kuiper

Open access · goldAbstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

5 authors at 3 institutions in 2 countries.

Eirini TsirvouliDepartment of Biology, Norwegian University of Science and Technology, 7034 Trondheim, Norway.
Vincent NoëlInstitut Curie, Université PSL, 75005 Paris, France.
Åsmund FlobakDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7030 Trondheim, Norway.
Laurence CalzoneInstitut Curie, Université PSL, 75005 Paris, France.
Martin KuiperDepartment of Biology, Norwegian University of Science and Technology, 7034 Trondheim, Norway.
Inserm · FRNorwegian University of Science and Technology · NOSINTEF · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis arises from complex interactions between keratinocytes and immune cells, leading to uncontrolled inflammation, immune hyperactivation, and a perturbed keratinocyte life cycle. Despite the availability of drugs for psoriasis management, the disease remains incurable. Treatment response variability calls for new tools and approaches to comprehend the mechanisms underlying disease development. We present a Boolean multiscale population model that captures the dynamics of cell-specific phenotypes in psoriasis, integrating discrete logical formalism and population dynamics simulations. Through simulations and network analysis, the model predictions suggest that targeting neutrophil activation in conjunction with inhibition of either prostaglandin E2 (PGE2) or STAT3 shows promise comparable to interleukin-17 (IL-17) inhibition, one of the most effective treatment options for moderate and severe cases. Our findings underscore the significance of considering complex intercellular interactions and intracellular signaling in psoriasis and highlight the importance of computational approaches in unraveling complex biological systems for drug target identification.

Indexed as

DiseaseDrugsMedicine

Identifiers

PMID38303723
PMCPMC10831929
OpenAlexW4390754123

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.