ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2022
Down-Regulation of miR-138 Alleviates Inflammatory Response and Promotes Wound Healing in Diabetic Foot Ulcer Rats via Activating PI3K/AKT Pathway and hTERT.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Insights Into Macrophage Polarization and M1/M2 Balance in Diabetic Foot Ulcers.Journal of diabetes · 2026Review
- FGFR2 is a Candidate Immune-Associated Marker of Diabetic Foot Ulcer That Promotes Keratinocyte Function by Activating the PI3K/Akt and MAPK Pathways.Mediators of inflammation · 2026Article
- Resistance Exercise Counteracts Skeletal Muscle Atrophy in T2DM Mice by Upregulating FGF21 and Activating PI3K/Akt Pathway.Biomolecules · 2025Article
- Targeting diabetic foot ulcer pathophysiology: altered signaling pathways and 3D scaffold as an emerging treatment strategy.3 Biotech · 2025Review
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- Inflammation-Modulating Biomedical Interventions for Diabetic Wound Healing: An Overview of Preclinical and Clinical Studies.ACS omega · 2024Review
- Combined with dynamic serum proteomics and clinical follow-up to screen the serum proteins to promote the healing of diabetic foot ulcer.Endocrine · 2024Article
- Curcumin Promotes Diabetic Foot Ulcer Wound Healing by Inhibiting miR-152-3p and Activating the FBN1/TGF-β Pathway.Molecular biotechnology · 2024Article
- Current status and progress in research on dressing management for diabetic foot ulcer.Frontiers in endocrinology · 2023Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To study the role of miR-138 on the repair of diabetic foot ulcer (DFU) and further to explore its possible mechanism. Materials and Methods: miR-138 inhibitor, IGF-1, LY294002 were used in DFU rat mode, and the mRNA expression of miR-138 was detected. HE staining was used to observe the histological changes of skin ulcer in rats. The level of inflammation, wound healing, and blood vessel formation-related factors were detected by ELISA and immunohistochemical. The expression of VEGF and PI3K/AKT pathway-related proteins were detected by Western blot. To further determine the underlying mechanism of miR-138 in the repair of DFU, telomerase inhibitor BIBR-1232 was used in HUVECs. Dual-luciferase assay was used to determine the target relationship between miR-138 and hTERT. CCK-8, transwell, and tube formation assays were conducted to observe the biological behavior of HUVECs. Inflammatory cytokines and PI3K/AKT pathway-related proteins were also measured by ELISA and Western blot. Results: The mRNA expression of miR-138 in DFU rat was increased and ulcer of diabetic foot rats was improved after silencing miR-138. The results of cellular bioactivity in vitro experiment were consistent with that in vivo. Meanwhile, after silencing miR-138, the level of inflammatory cytokines was decreased, while the level of anti-inflammatory and healing factors was increased in vivo and vitro. Moreover, the ratios of p-PI3K/PI3K and p-AKT/AKT were upregulated after treated with miR-138 inhibitor and miR-138 was negatively regulated the expression of hTERT. However, the inhibitory effect on inflammatory response and the promotion effect on wound healing of miR-138 inhibitor were reversed by LY294002 and BIBR-1232. Conclusion: Down-regulation of miR-138 could alleviate inflammatory response and promote wound healing in DFU rats by activating PI3K/AKT pathway and hTERT.
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