ArticleSkin health and disease2022
Abnormal keratin expression pattern in prurigo nodularis epidermis.
Article in Skin health and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Insight into Apert Syndrome: Reporting on Six Patients and Increasing Awareness.Molecular neurobiology · 2025Article
- A murine model of prurigo nodularis-like skin lesions induced by persistent scratching under type 2 inflammatory conditions.Frontiers in immunology · 2025Article
- Keratins 6, 16, and 17 in Health and Disease: A Summary of Recent Findings.Current issues in molecular biology · 2024Review
- Chronic Nodular Prurigo: An Update on the Pathogenesis and Treatment.International journal of molecular sciences · 2022Review
- Abnormal keratin expression pattern in prurigo nodularis epidermis.Skin health and disease · 2022Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Prurigo nodularis (PN) is a highly pruritic, chronic dermatosis and difficult to treat. PN lesions are characterized by existence of many hyperkeratotic, erosive papules and nodules. However, the pathogenesis of PN still remains unelucidated. Aim: To clarify the keratin role in the epidermis hyperproliferation, the keratin expression pattern in the PN lesional skin. Methods: In this study, we enrolled 24 patients with PN and 9 healthy control volunteers. K1/K10, K5/K14, K6/K16/K17 expression pattern were investigated by using immunohistochemical staining. Results: The lesional skin consists of the thickened spinous layers, in which active cell division was found. K5/K14 were upregulated in PN lesional epidermis, the staining signal localized in the basal layer and lower suprabasal layers. Hyperproliferation-associated K6 was found in all layers of epidermal lesional skin, especially in the spinous layers. In contrast, K16 was only detected in the basal and lower suprabasal layers, K17 was observed in the basal and spinous layers. Terminal differential keratins K1/K10 were upregulated, detected in the pan-epidermis, but spared in the basal and low suprabasal layers. Conclusion: The keratinocytes enter an alternative differentiation pathway, which are responsible for the activated keratinocyte phenotype, abnormal keratins expression potentially contributes to the keratinocytes proliferation, subsequently lead to increased lesional skin epidermis thickness, hyperkeratiosis and alteration of skin barrier properties.
Identifiers
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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.