ReviewPsoriasis (Auckland, N.Z.)2022
Updated Perspectives on Keratinocytes and Psoriasis: Keratinocytes are More Than Innocent Bystanders.
Review in Psoriasis (Auckland, N.Z.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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.
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.
Who cites it
56 citing papers in PubMed, 76 citations in OpenAlex.
- Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation.Pharmaceutical biology · 2026Article
- GS-9620 alleviates psoriasis-like inflammation by regulating autophagy in keratinocytes.Animal models and experimental medicine · 2026Article
- Hesperidin methyl chalcone alleviates imiquimod-induced psoriasis in mice: effects alone and in combination with methotrexate.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Calcium signaling in psoriasis: from pathogenesis to therapeutic opportunities.Frontiers in immunology · 2026Review
- Interferon regulatory factor 4 as a context-dependent regulator of inflammation: transcriptional and epigenetic control, skin diseases, and translational challenges.Frontiers in immunology · 2026Review
- Integrating bulk RNA-seq, Mendelian randomization and single-cell RNA-seq to elucidate the roles of lactate metabolism related markers-SLC25A4 and keratinocyte in the pathogenesis of psoriasis.Frontiers in immunology · 2026Article
- Role of dendritic cells and B cells in the skin of imiquimod (IMQ)-induced psoriasis-like mouse model.PeerJ · 2026Article
- Psoriasis: microbiome dysbiosis and pathogenic mechanisms.Frontiers in immunology · 2026Review
- Skin delivery and anti-inflammatory effects of the anesthetic propofol against psoriasiform lesions through KEAP1/Nrf2/HO-1 pathway activation.Cellular and molecular life sciences : CMLS · 2025Article
- Balancing efficacy and hepatotoxicity: a comprehensive review of oral medications in psoriasis management.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Modulation of Nuclear Factor Kappa B Signaling and microRNA Profiles by Adalimumab in LPS-Stimulated Keratinocytes.International journal of molecular sciences · 2025Article
- The role of the mineralocorticoid receptor in skin.Molecular and cellular endocrinology · 2025Review
- The dual roles of T cells and keratinocytes in seborrheic dermatitis: a narrative review.European journal of medical research · 2025Review
- The alleviating effect of Bai-Ju essence on atopic dermatitis through anti-inflammatory and skin barrier repair mechanisms.Molecular and cellular biochemistry · 2025Article
- Harnessing Quinone Derivatives fromACS pharmacology & translational science · 2025Article
- The M2 Macrophages Importance Role in Psoriasis.Immunity, inflammation and disease · 2025Review
- Oral and topical vitamin D treatment strategies in psoriasis.Skin health and disease · 2025Review
- Tapinarof Nanogels as a Promising Therapeutic Approach.Pharmaceutics · 2025Review
- Aquaporin 3 inhibition attenuates imiquimod-induced psoriatic symptoms in a murine model.Molecular biology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Psoriasis is a complex disease triggered by genetic, immunologic, and environmental stimuli. Many genes have been linked to psoriasis, like the psoriasis susceptibility genes, some of which are critical in keratinocyte biology and epidermal barrier function. Still, the exact pathogenesis of psoriasis is unknown. In the disease, the balance between the proliferative and differentiative processes of keratinocytes becomes altered. Multiple studies have highlighted the role of dysregulated immune cells in provoking the inflammatory responses seen in psoriasis. In addition to immune cells, accumulating evidence shows that keratinocytes are involved in psoriasis pathogenesis, as discussed in this review. Although certain immune cell-derived factors stimulate keratinocyte hyperproliferation, activated keratinocytes can also produce anti-microbial peptides, cytokines, and chemokines that can promote their proliferation, as well as recruit immune cells to help initiate and reinforce inflammatory feedback loops. Psoriatic keratinocytes also show intrinsic differences from normal keratinocytes even after removal from the in vivo inflammatory environment; thus, psoriatic keratinocytes have been found to exhibit abnormal calcium metabolism and possible epigenetic changes that contribute to psoriasis. The Koebner phenomenon, in which injury promotes the development of psoriatic lesions, also provides evidence for keratinocytes' contributions to disease pathogenesis. Furthermore, transgenic mouse studies have confirmed the importance of keratinocytes in the etiology of psoriasis. Finally, in addition to immune cells and keratinocytes, data in the literature support roles for other cell types, tissues, and systems in psoriasis development. These other contributors are all potential targets for therapies, suggesting the importance of a holistic approach when treating psoriasis.
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What Socratic holds
Registered trials
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.