ArticleInternational wound journal2013
Chronic wounds - is cellular 'reception' at fault? Examining integrins and intracellular signalling.
Article in International wound journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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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
16 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- An Update on the Correlation Between Neuroimmunomodulation, Photodynamic Therapy (PDT), and Wound Healing: The Role of Mast Cells.Biomedicines · 2026Review
- Idiopathic pulmonary fibrosis (IPF): disease pathophysiology, targets, and potential therapeutic interventions.Molecular and cellular biochemistry · 2024Review
- Spatially resolved metabolomics visualizes heterogeneous distribution of metabolites in lung tissue and the anti-pulmonary fibrosis effect ofJournal of pharmaceutical analysis · 2024Article
- ROS-scavenging materials for skin wound healing: advancements and applications.Frontiers in bioengineering and biotechnology · 2023Review
- Mesenchymal stromal cells promote the proliferation of basal stem cells and efficient epithelization in organotypic models of wound healing.Microscopy research and technique · 2022Article
- Biome-microbiome interactions in peri-implantitis: A pilot investigation.Journal of periodontology · 2022Article
- Time-dependent changes in extra-domain A-fibronectin concentration and relative amounts of fibronectin-fibrin complexes in plasma of patients with peripheral arterial disease after endovascular revascularisation.International wound journal · 2018Article
- In vitro assessment of a novel, hypothermically stored amniotic membrane for use in a chronic wound environment.International wound journal · 2017Article
- Integrin-mediated regulation of epidermal wound functions.Cell and tissue research · 2016Review
- Adipose-derived stem cells and keratinocytes in a chronic wound cell culture model: the role of hydroxyectoine.International wound journal · 2015Article
- Integrins in Wound Healing.Advances in wound care · 2014Review
- Non-thermal atmospheric-pressure plasma possible application in wound healing.Biomolecules & therapeutics · 2014Review
- Fibronectin in tissue regeneration: timely disassembly of the scaffold is necessary to complete the build.Cellular and molecular life sciences : CMLS · 2013Review
- Integrins as Modulators of Transforming Growth Factor Beta Signaling in Dermal Fibroblasts During Skin Regeneration After Injury.Advances in wound care · 2013Review
- Differential influence of components resulting from atmospheric-pressure plasma on integrin expression of human HaCaT keratinocytes.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As with all physiologic processes, chronic wounds are associated with unique intracellular and cellular/extracellular matrix (ECM) receptor types and signalling messages. These cellular receptors mediate responses of the epidermis to provisional wound matrix and change in form and number in cases of impaired wound healing. Integrins are the major cell-surface receptors for cell adhesion and migration and epidermal keratinocytes express several integrins that bind ECM ligands in provisional wound ECM. Integrin receptors and more particularly integrin clusters and focal adhesion points appear to influence epidermal and dermal cell matrix interactions, cell motility, cell phenotype and ultimate healing trajectory. In chronic wounds, a variety of changes in receptors have been identified: decreased integrin α5β1 receptors affect the integration of fibronectin and subsequent keratinocyte migration; integrin αvβ6 stimulate transforming growth factor (TGF)-β and may increase the susceptibility to ulceration and fibrosis; however, TGF-β signal receptors have been found to be dysfunctional in many chronic wounds; additionally receptor interactions result in increased senescent cells including fibroblasts, myofibroblasts and even keratinocytes - this produces a degradative ECM and wound bed and corrosive chronic wound fluid. The activation or inhibition of integrin receptors by various agents may provide an excellent means of influencing wound healing. This process offers an earlier intervention into the wound healing cascade promoting intrinsic healing and elaboration of growth factors and ECM proteins, which may be more cost effective than the traditional attempts at extrinsic addition of these agents.
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