Evidence map›Paper›PMID 40571687›Full record

ReviewNature reviews. Disease primers2025

Psoriasis.

April W Armstrong, Andrew Blauvelt, Kristina Callis Duffin, Yu-Huei Huang, Laura J Savage, Lily Guo, Joseph F Merola

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Disease primers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

129 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Phase 1 study of balinatunfib, an oral inhibitor of TNFR1 signal in mild-to-moderate psoriasis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Trial
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. LCN2-Driven Fibroblast Ferroptosis-Associated Injury Promotes Keratinocyte Proliferation via Lipid Peroxidation Signaling in Psoriasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  19. TopicalPharmaceutics · 2026
    Article
  20. Article

69 more citing papers are in PubMed but not listed here.

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.

April W ArmstrongDivision of Dermatology, Department of Medicine, University of California Los Angeles David Geffen School of Medicine, Los Angeles, CA, USA. armstrongpublication@gmail.com.ORCID http://orcid.org/0000-0003-0064-8707
Andrew BlauveltBlauvelt Consulting LLC, Annapolis, MD, USA.ORCID http://orcid.org/0000-0002-2633-985X
Kristina Callis DuffinDepartment of Dermatology, University of Utah Spencer F. Eccles School of Medicine, Salt Lake City, UT, USA.
Yu-Huei HuangDepartment of Dermatology, Chang Gung Memorial Hospital and College of Medicine, Chang Gung University, Taoyuan City, Taiwan.
Laura J SavageLeeds Centre for Dermatology, University of Leeds, Leeds, UK.
Lily GuoDuke University School of Medicine, Durham, NC, USA.
Joseph F MerolaDepartment of Dermatology, UT Southwestern Medical Center, Dallas, TX, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plaque psoriasis is a chronic, immune-mediated inflammatory skin disease that has considerable effects on patients' physical, psychological and social well-being. It is strongly influenced by genetic predisposition, with HLA-C*06:02 showing the strongest association, particularly in those with early-onset disease. Additional susceptibility loci, including IL23A, IL12B and IL17RA, are linked to dysregulation of the IL-23-T helper 17 axis, which contributes to chronic inflammation and keratinocyte hyperproliferation. Plaque psoriasis is frequently associated with psoriatic arthritis and other comorbidities, such as cardiovascular disease, metabolic syndrome and psychiatric disorders, all of which contribute to increased morbidity and mortality. Management strategies are tailored to disease severity and the presence of comorbidities. For mild disease, topical therapies remain the first-line treatment, including corticosteroids, vitamin D analogues and topical calcineurin inhibitors. New non-steroidal agents, such as topical PDE4 and aryl hydrocarbon receptor agonists, offer additional options. In moderate-to-severe disease, oral systemic therapies, such as methotrexate, ciclosporin, acitretin, apremilast and deucravacitinib, provide a range of immunomodulatory effects. Biologic therapies targeting TNF, IL-17, IL-23 and IL-12/23 have demonstrated high efficacy in improving both cutaneous and systemic inflammation. Current research on systemic therapies is focused on the development of additional inhibitors of the Tyk2 pathway and inhibitors to IL-23 receptor, IL-17, and TNF. Early screening for psoriatic arthritis, proactive cardiovascular risk reduction and multidisciplinary care are crucial to optimizing long-term outcomes. Ongoing research continues to advance precision medicine approaches, with the goal of enhancing treatment durability and improving quality of life for individuals living with psoriasis.

Indexed as

PsoriasisArthritis, PsoriaticHumans

Identifiers

PMID40571687

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.