ArticleMedComm2025
Cuproptosis Facilitates Chronic Skin Inflammation by Regulating the α-Ketoglutarate/H3K4me3/Ferritin Heavy Chain 1 Signaling Pathway-Mediated Ferroptosis.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- Effects of cuproptosis and its application in inflammatory bowel disease (Review).International journal of molecular medicine · 2026Review
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Metal oxide nanoparticles for acne vulgaris: mechanisms, synthesis, formulation, and translational prospects.RSC advances · 2026Review
- Deciphering the rules of regulated cell death subroutines by in silico methods.Journal of advanced research · 2026Review
- From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4.Redox biology · 2026Article
- Transdermal siRNA delivery via biomineralized nanoparticle-incorporated microneedles modulates cuproptosis-ferroptosis interaction for psoriasis therapy.Materials today. Bio · 2026Article
- The metabolite α-ketoglutarate induces AIM2-dependent PANoptosis through demethylase TET2.Cell communication and signaling : CCS · 2026Article
- DHA Targets RAB1B to Mediate the Driving Force Transmission of Copper Ion Vesicular Endocytosis Under Copper Overload for Promoting Cuproptosis and Ferroptosis in Hepatic Stellate Cells.International journal of biological sciences · 2026Article
- SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism.Frontiers in immunology · 2026Article
- Ferroptosis as an Emerging Therapeutic Target in Allergic Diseases.Drug design, development and therapy · 2026Review
- Redox Network Dysfunction: Integrating Ferroptosis and Cuproptosis Across Human Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Activation of NF-κB signaling in tissue-resident memory T cells promotes recurrent psoriasis in mice.Frontiers in immunology · 2025Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated copper homeostasis is implicated in inflammatory skin diseases such as psoriasis and atopic dermatitis (AD), but the role of cuproptosis remains poorly defined. This study aimed to elucidate the role and mechanism of cuproptosis in inflammatory skin diseases. Transcriptome analysis of patient lesions revealed significant alterations in cuproptosis-related genes correlating with disease-specific pathological features. These cuproptosis-related gene expression signatures demonstrated strong clinical relevance to therapeutic efficacy in both psoriasis and AD cohorts. Functional validation using disease models showed that pharmacologically inhibiting cuproptosis with the copper chelator tetrathiomolybdate (TTM), or genetically knocking down the copper importer SLC31A1, effectively alleviated chronic skin inflammation and hallmark pathological changes induced by imiquimod (IMQ) or calcipotriol (MC903). Mechanistically, we uncovered that SLC31A1-mediated cuproptosis promotes intracellular α-ketoglutarate (α-KG) accumulation, driving activation of the lysine demethylase KDM5B. Activated KDM5B specifically demethylates H3K4me3 marks at the promoter of the ferroptosis regulator ferritin heavy chain 1 (FTH1), suppressing its transcription and consequently sensitizing keratinocytes to ferroptotic cell death, thereby amplifying inflammatory tissue damage. Our findings establish a fundamental pathogenic SLC31A1/KDM5B/FTH1 molecular axis linking dysregulated copper metabolism and cuproptosis to ferroptosis execution in psoriasis and AD, providing significant mechanistic insights and pinpointing promising therapeutic targets for these refractory skin disorders.
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