ReviewPsoriasis (Auckland, N.Z.)2024
Research Progress on Glycolysis Mechanism of Psoriasis.
Review in Psoriasis (Auckland, N.Z.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2-Mediated Glycolysis in Keratinocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Role of Disulfidptosis in the Local Inflammatory Response of Atopic Dermatitis.Clinical and translational allergy · 2026Article
- Review
- Proteomic Identification of PFKFB3 and PFKFB4 Associated with Coenzyme Metabolism and Redox Imbalance in Dairy Cows with Clinical Mastitis.Antioxidants (Basel, Switzerland) · 2026Article
- Anti-cancer Mechanisms and Applications of Cinnamon Extract: A Comprehensive Review.Chinese journal of integrative medicine · 2026Review
- Machine learning meets psoriasis: identifying key lactylation biomarkers as potential targets for diagnosis and therapies.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory disease with a complex pathogenesis. Hyperplasia of glycolytic-dependent epidermal keratinocytes (KCs) is a new hallmark of psoriasis pathogenesis. Meanwhile, immune cells undergo metabolic reprogramming similar to KCs. Glycolysis provides energy for the proliferation of KCs, while it also releases lactic acid to facilitate the differentiation of immune cells. In turn, differentiated immune cells further promote KCs glycolysis by releasing inflammatory factors, thus forming an immunometabolism loop. The interaction between immune response and metabolic pathways jointly promotes the sustained proliferation of KCs and the secretion of various inflammatory factors by immune cells. Understanding the role of glycolysis in immunometabolism of psoriasis may provide new ideas for non-immunosuppressive treatment of psoriasis. This article aims to review the role of glycolysis in the pathogenesis of psoriasis and attempts to summarize the key enzymes and regulatory factors involved in psoriasis glycolysis, as well as their interactions. Finally, we discuss the pharmacological modulators of glycolysis in psoriasis.
Indexed as
Identifiers
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.