ArticleInternational journal of medical sciences2024
miR-758-3p/ILK signaling modulated angiogenesis by regulating VEGFA in wound healing.
Article in International journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Natural Polysaccharide-Based Biomaterials for Skin Wound Healing: Immunomodulatory Mechanisms and Macrophage M2 Polarization.Gels (Basel, Switzerland) · 2026Review
- Review
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic wounds cause physical, psychological and economic damage to patients, while therapeutic choices are limited. ILK was reported to play key roles in both fibrosis and angiogenesis, which are two important factors during wound healing. However, the function of ILK during vascularization in wounds remains unclear. In our study, we found increased ILK expression in chronic wound tissues compared to adjacent tissue, as well as a positive relationship between ILK expression and microvessel density. Moreover, fibroblasts overexpressing ILK showed an enhanced ability to promote HUVEC migration and tube formation, during which PI3K/Akt, downstream of ILK, played key roles and VEGFA was the key cytokine. Considering the important function of ILK in wound healing and the lack of an ILK activator, we investigated microRNAs targeting ILK and found that miR-758-3p could target ILK to regulate its transcription. The inhibition of miR-758-3p increased ILK expression and sequentially upregulated VEGFA and activated angiogenesis
Indexed as
Identifiers
What OpenQuestion holds
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.