ArticleApplied biochemistry and biotechnology2024
Inhibition of Integrin-Associated Kinases FAK and ILK on the In Vitro Model of Skin Wound Healing.
Article in Applied biochemistry and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 3 citations in OpenAlex.
- Integrin-linked kinase promotes hepatic fat accumulation via F-actin stabilization-dependent CD36 plasma membrane localization.iScience · 2026Article
- Smart colorimetric wound dressing for real-time infection detection and monitoring.Journal of biological engineering · 2026Review
- Autophagy-Ferroptosis Interplay Network: Redefining Therapeutic Paradigms for Diabetic Wound Healing.Journal of inflammation research · 2026Review
- Neutrophil Heterogeneity in Wound Healing.Biomedicines · 2025Review
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Authors and funding
1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Dermal fibroblasts are essential cells of skin tissue responsible for its normal functioning. In skin wounds, the differentiation of resident fibroblasts into myofibroblasts occurs, which is accompanied by the rearrangement of actin cytoskeleton with the expression of alpha-smooth muscle actin. This transformation is a prerequisite for a successful wound healing. At the same time, different studies indicate that extracellular matrix may be involved in regulation of this process. Since the connection between cells and matrix is provided by transmembrane integrin receptors, this work was aimed at studying the dynamics of signaling pathways associated with integrins on an in vitro model of wound healing using human skin fibroblasts. It was shown that the healing of simulated wound was accompanied by a change in the level of integrins as well as integrin-associated kinases ILK (integrin-linked kinase) and FAK (focal adhesion kinase). Pharmacological inhibition of ILK and FAK caused the suppression of p38 and Akt which proteins are involved in regulation of the actin cytoskeleton. Moreover, it resulted in an inefficient wound closure in vitro. The results of this study support the involvement of integrin-associated kinases in regulation of fibroblast-to-myofibroblast transition during wound healing.
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