ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2023
NKG2D Ligand Expression Induced by Oxidative Stress Mitigates Cutaneous Ischemia-Reperfusion Injury.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Circulating natural killer cells are phenotypically and functionally altered in age-related macular degeneration.Cell reports. Medicine · 2026Article
- Identification of a Diagnostic Gene Signature Associated with Centrosome Amplification in Pressure Injuries: A Cross-Sectional Transcriptome and Machine Learning Study.Journal of inflammation research · 2026Article
- Extracellular CIRP augments inflammation in acute kidney injury via NKG2D-positive macrophages.Frontiers in immunology · 2025Article
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Authors and funding
5 authors.
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Abstract
Pressure ulcers represent a crucial clinical problem, especially in hospitalized patients. Ischemia-reperfusion (I-R) is an important cause of these lesions. Natural killer (NK), invariant NK T (iNKT), and dendritic epidermal T-cells, which express the natural killer group 2, member D (NKG2D) receptor, have been reported to have physiological roles in skin tissue repair and wound healing. However, a role for NKG2D-NKG2D ligand interactions in I-R-induced skin injury has not been determined. Using a murine pressure ulcer model, we demonstrated that I-R-induced ulcers in NKG2D-deficient mice were larger than those in wild-type or T-cell receptor δ knockout mice. Histopathological evaluation revealed that accumulation of macrophages and neutrophils at the peripheral deep dermis and subcutaneous tissue of the ulcers was enhanced in NKG2D-deficient mice.
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Registered trials
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