ArticleResearch (Washington, D.C.)2023
CD147 Facilitates the Pathogenesis of Psoriasis through Glycolysis and H3K9me3 Modification in Keratinocytes.
Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled 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.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- New hope for the treatment of recurrent and refractory psoriasis: NK cell immunotherapy-A scientometric analysis.Frontiers in immunology · 2025Pooled it
- Reshaping psoriasis topical therapy: Continuous hydrogenation orchestrates 'redox-metabolic homeostasis' for efficient remission and relapse intervention.Bioactive materials · 2026Article
- Multi‑omics and their integration in psoriasis research (Review).Molecular medicine reports · 2026Review
- Identification of UBE2T as a novel diagnostic biomarker of psoriasis and proliferating UBE2T+ Keratinocyte in psoriasis.Journal of translational medicine · 2026Article
- Inducible CD147 up-regulation boosts extended SARS-CoV-2 infection triggering severe COVID-19 independent of ACE2.Signal transduction and targeted therapy · 2026Article
- CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Genetic analysis of potential biomarkers and therapeutic targets in hypoxia and pyroptosis from psoriasis.Biochemistry and biophysics reports · 2025Article
- Article
- Crotonylation deficiency of S100A7 K49 promotes psoriatic keratinocyte proliferation through enhanced interaction with RAGE.Scientific reports · 2025Article
- Immunological profile of lactate metabolism-related genes in Psoriasis a comprehensive analysis based on bulk and single-cell RNA sequencing data.Scientific reports · 2025Article
- Lactylation-Boosted mResearch (Washington, D.C.) · 2025Article
- Direct Identification of O-Glycopeptides by Low-Temperature Assisted Nanopore Technique.Research (Washington, D.C.) · 2025Article
- Stromal cells and epigenetics: emerging key players of chronic inflammatory skin diseases.BMB reports · 2024Review
- IL-17A Orchestrates Reactive Oxygen Species/HIF1α-Mediated Metabolic Reprogramming in Psoriasis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Energy competition remodels the metabolic glucose landscape of psoriatic epidermal cells.Theranostics · 2024Article
- Melatonergic Signaling Sustains Food Allergy Through FcεRI Recycling.Research (Washington, D.C.) · 2024Article
- Aggregation-Induced Emission-Active Photosensitizer-Mediated Photodynamic Therapy for Anti-Psoriasis.Research (Washington, D.C.) · 2024Article
- Research Progress on Glycolysis Mechanism of Psoriasis.Psoriasis (Auckland, N.Z.) · 2024Review
- CD147/Basigin Is Involved in the Development of Malignant Tumors and T-Cell-Mediated Immunological Disorders via Regulation of Glycolysis.International journal of molecular sciences · 2023Review
- Noval advance of histone modification in inflammatory skin diseases and related treatment methods.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disease featuring rapid proliferation of epidermal cells. Although elevated glycolysis flux has been reported in psoriasis, the molecular mechanisms underlying its pathogenesis remain unclear. We investigated the role of the integral membrane protein CD147 in psoriasis pathogenesis, observing its high expression in psoriatic skin lesions of humans and imiquimod (IMQ)-induced mouse models. In mouse models, genomic deletion of epidermal CD147 markedly attenuated IMQ-induced psoriatic inflammation. We found that CD147 interacted with glucose transporter 1 (Glut1). Depletion of CD147 in the epidermis blocked glucose uptake and glycolysis in vitro and in vivo. In CD147-knockout mice and keratinocytes, oxidative phosphorylation was increased in the epidermis, indicating CD147's pivotal role in glycolysis reprogramming during pathogenesis of psoriasis. Using non-targeted and targeted metabolic techniques, we found that epidermal deletion of CD147 significantly increased the production of carnitine and α-ketoglutaric acid (α-KG). Depletion of CD147 also increased transcriptional expression and activity of γ-butyrobetaine hydroxylase (γ-BBD/
Identifiers
What OpenQuestion 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 OpenQuestion graph.