ArticleScientific reports2023
Different molecular pathways are disrupted in Pyoderma gangrenosum patients and are associated with the severity of the disease.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Pyoderma gangrenosum: a case report highlighting the importance of early diagnosis and treatment.International journal of surgery case reports · 2026Article
- Pyoderma gangrenosum: pathogenetic mechanisms and their implications for treatment.Seminars in immunopathology · 2025Review
- Disrupted Redox Regulation and Inflammatory Response in Pyoderma Gangrenosum.Life (Basel, Switzerland) · 2025Article
- Gasdermin D-dependent neutrophil extracellular traps exacerbate cytokine storm contributing to pyoderma gangrenosum pathogenesis.iScience · 2025Article
- Case Report: Spesolimab for pyoderma gangrenosum in an undifferentiated oligoarthritis patient receiving anti-IL-17 therapy.Frontiers in immunology · 2025Article
- The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives.International journal of molecular sciences · 2024Review
- New treatment of pyoderma gangrenosum and hidradenitis suppurativa: A review.The Journal of dermatology · 2024Review
- What can inherited immunodeficiencies reveal about pyoderma gangrenosum?Experimental dermatology · 2024Review
- Pyoderma Gangrenosum: Treatment Options.Drugs · 2023Review
- Pyoderma gangrenosum following anti-TNF therapy in chronic recurrent multifocal osteomyelitis: drug reaction or cutaneous manifestation of the disease? A critical review on the topic with an emblematic case report.Frontiers in medicine · 2023Review
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Authors and funding
8 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pyoderma gangrenosum (PG) is a rare inflammatory skin disease classified within the spectrum of neutrophilic dermatoses. The pathophysiology of PG is yet incompletely understood but a prominent role of genetics facilitating immune dysregulation has been proposed. This study investigated the potential contribution of disrupted molecular pathways in determining the susceptibility and clinical severity of PG. Variant Enrichment Analysis, a bioinformatic pipeline applicable for Whole Exome Sequencing data was performed in unrelated PG patients. Eleven patients were enrolled, including 5 with unilesional and 6 with multilesional PG. Fourteen pathways were exclusively enriched in the "multilesional" group, mainly related to immune system (i.e., type I interferon signaling pathway), cell metabolism and structural functions. In the "unilesional" group, nine pathways were found to be exclusively enriched, mostly related to cell signaling and cell metabolism. Genetically altered pathways involved in immune system biology and wound repair appear to be nodal pathogenic drivers in PG pathogenesis.
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