ArticlePloS one2013
Deep tissue injury in development of pressure ulcers: a decrease of inflammasome activation and changes in human skin morphology in response to aging and mechanical load.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 77 citations in OpenAlex.
- Targeting the NOD-Like Receptor Pyrin Domain Containing 3 Inflammasome to Improve Healing of Diabetic Wounds.Advances in wound care · 2023Review
- Recombinant GM-CSF for diseases of GM-CSF insufficiency: Correcting dysfunctional mononuclear phagocyte disorders.Frontiers in immunology · 2022Review
- Polylysine for skin regeneration: A review of recent advances and future perspectives.Bioengineering & translational medicine · 2022Review
- The Role of Extracellular Matrix in Skin Wound Healing.Journal of clinical medicine · 2021Review
- Pressure injuries during the SARS-CoV-2 pandemic: A retrospective, case-control study.Journal of tissue viability · 2021Article
- Experimental animal modelling for pressure injury: A systematic review.Journal of clinical orthopaedics and trauma · 2021Review
- Mechanosensitive Piezo1 Channel Evoked-Mechanical Signals in Atherosclerosis.Journal of inflammation research · 2021Review
- Changes in the three-dimensional microscale topography of human skin with aging impact its mechanical and tribological behavior.PloS one · 2021Article
- Photobiomodulation by dual-wavelength low-power laser effects on infected pressure ulcers.Lasers in medical science · 2020Article
- An Experimental Intervention Study Assessing the Impact of a Thin Silicone Gel Surface Overlay on Interface Pressure.Radiology research and practice · 2020Article
- A narrative review on pressure ulcer (PU) studies relevant to medical imaging.The Pan African medical journal · 2020Review
- [The Hospital Admision Register (CMBD) use for the analisys of hospital aquired pressure ulcer at the region of Valencia (2012-2015)].Revista espanola de salud publica · 2019Article
- Two-Hourly Repositioning for Prevention of Pressure Ulcers in the Elderly: Patient Safety or Elder Abuse?Journal of bioethical inquiry · 2019Article
- Mechanical regulation of macrophage function - cyclic tensile force inhibits NLRP3 inflammasome-dependent IL-1β secretion in murine macrophages.Inflammation and regeneration · 2019Review
- Ablation of Bax and Bak protects skeletal muscle against pressure-induced injury.Scientific reports · 2018Article
- Opportunities for organoids as new models of aging.The Journal of cell biology · 2018Review
- Contribution of the inflammasome to inflammaging.Journal of inflammation (London, England) · 2018Article
- A Novel Silver Bioactive Glass Elicits Antimicrobial Efficacy AgainstFrontiers in microbiology · 2018Article
- Acidification changes affect the inflammasome in human nucleus pulposus cells.Journal of inflammation (London, England) · 2016Article
- Analysis of Gene Expression in Experimental Pressure Ulcers in the Rat with Special Reference to Inflammatory Cytokines.PloS one · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Molecular mechanisms leading to pressure ulcer development are scarce in spite of high mortality of patients. Development of pressure ulcers that is initially observed as deep tissue injury is multifactorial. We postulate that biomechanical forces and inflammasome activation, together with ischemia and aging, may play a role in pressure ulcer development. To test this we used a newly-developed bio-mechanical model in which ischemic young and aged human skin was subjected to a constant physiological compressive stress (load) of 300 kPa (determined by pressure plate analyses of a person in a reclining position) for 0.5-4 hours. Collagen orientation was assessed using polarized light, whereas inflammasome proteins were quantified by immunoblotting. Loaded skin showed marked changes in morphology and NLRP3 inflammasome protein expression. Sub-epidermal separations and altered orientation of collagen fibers were observed in aged skin at earlier time points. Aged skin showed significant decreases in the levels of NLRP3 inflammasome proteins. Loading did not alter NLRP3 inflammasome proteins expression in aged skin, whereas it significantly increased their levels in young skin. We conclude that aging contributes to rapid morphological changes and decrease in inflammasome proteins in response to tissue damage, suggesting that a decline in the innate inflammatory response in elderly skin could contribute to pressure ulcer pathogenesis. Observed morphological changes suggest that tissue damage upon loading may not be entirely preventable. Furthermore, newly developed model described here may be very useful in understanding the mechanisms of deep tissue injury that may lead towards development of pressure ulcers.
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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.