ArticleInternational wound journal2021
Cellular and molecular changes that predispose skin in chronic spinal cord injury to pressure ulcer formation.
Article in International wound journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Skin and tissue changes after spinal cord injury-A scoping review.Spinal cord series and cases · 2026Article
- Molecular Pathophysiology of Chronic Wounds: Current State and Future Directions.Cold Spring Harbor perspectives in biology · 2023Review
- Cellular and molecular changes that predispose skin in chronic spinal cord injury to pressure ulcer formation.International wound journal · 2021Article
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 at 2 institutions in 1 country.
Funding
Abstract
Patients with spinal cord injury have a predisposition to develop pressure ulcers. Specific characteristics of the patients' skin potentially involved have not yet been identified. The purpose of this investigation was to determine whether loss of neuronal control affects cellular and molecular homeostasis in the skin. Intact afflicted skin, wound edge of pressure ulcers, and control skin were analysed. Platelets, transforming growth factor-β1, and activin A were identified by immunohistochemistry. Transforming growth factor-β-like activity was determined by bioassay, and gene expression by DNA microarray analysis or RT-PCR. In afflicted skin, enhanced platelet extravasation was detected. Transforming growth factor-β1 and activin A accumulated in the dermal-epidermal junction zone. Transforming growth factor-β-like activity and activin A expression were increased in intact afflicted skin (compared to control skin) and were further enhanced in pressure ulcers. In vitro, activity was generated by fibroblast-epithelial cell interactions, which also induced activin A. Thus, loss of neuronal control in spinal cord injury appears to trigger inappropriate wound healing processes in the patients' skin. Plasma leakage and increased transforming growth factor-β-like activity combined with shear forces potentially enhance the risk for pressure ulcer formation.
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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.