ArticleHeliyon2022
Hypoxic preconditioning promotes galvanotaxis of human dermal microvascular endothelial cells through NF-κB pathway.
Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- A multi therapy bioelectronic wound dressing.npj biomedical innovations · 2026Article
- Electrical Stimulation Therapy - Dedicated to the Perfect Plastic Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis plays an important role in wound healing, especially in chronic wound. The directional migration of the human dermal microvascular endothelial cells (HDMECs) is the key regulation of angiogenesis. The wound healing can be regulated by numerous microenvironment factors including the electric fields, hypoxia and chemotaxis. During wound repair, the electric fields mediates the directional migration of cells and the hypoxia, which occurs immediately after injury, acts as an early stimulus to initiate the healing process. However, the mechanism of hypoxia and the endogenous electric fields coordinating to promote angiogenesis remain elusive. In this study, we observed the effect of hypoxia on the directional migration of HDMECs under electric fields. The galvanotaxis of HDMECs under the electric fields (200 mV/mm) was significantly improved, and the expression of VEGF/VEGFR2 was up-regulated after 4h of hypoxic preconditioning. In addition, the knockdown of VEGFR2 reversed the directivity of HDMECs promoted by hypoxia in the electric fields. Moreover, knockdown of VEGFR2 inhibited the migration directionality of HDMECs in the electric field after hypoxic preconditioning. Hypoxia decreased the activation of NF-κB in HDMECs. Activated NF-κB by fusicoccin decreased the expression of VEGFR2/VEGF and negatively regulated the migration direction of HDMECs in the electric fields. Enhancing the galvanotaxis response of cells might therefore be a clinically attractive approach to induce improved angiogenesis.
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Registered trials
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