ArticleJournal of translational medicine2024
METTL3-mediated NDUFB5 m6A modification promotes cell migration and mitochondrial respiration to promote the wound healing of diabetic foot ulcer.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Licoisoflavone A ameliorates adipose tissue dysfunction in diet‑induced obesity by promoting METTL3 expression.Molecular medicine reports · 2026Article
- Bone Marrow Mesenchymal Stem Cells Rescue Tendon Injury by Regulating FTO-Mediated m6A Methylation of ELOB.Journal of biochemical and molecular toxicology · 2026Article
- WTAP-mediated m6A RNA methylation promotes diabetic foot ulcer healing under negative pressure wound therapy.Journal of diabetes investigation · 2026Article
- Dynamic matrix engineering promotes nascent protein deposition to drive cell migration and expedite Re-epithelization in chronic wound.Bioactive materials · 2026Article
- Mitochondrion-targeted therapies for diabetic wound healing: from mechanism to therapeutic opportunity.Burns & trauma · 2026Review
- RNA modifications: molecular orchestrators of wound healing.Burns & trauma · 2026Article
- Activated oligoadenylate synthetase-ribonuclease L pathway promotes endothelial pyroptosis and impairs diabetic wound healing via thioredoxin-interacting protein mMolecular biomedicine · 2025Article
- Regulation of m6A methylation in the immune microenvironment in the development of diabetes mellitus.Journal of translational medicine · 2025Review
- Review
- Mitochondrial medicine: "from bench to bedside" 3PM-guided concept.The EPMA journal · 2025Article
- ALKBH3-Mediated MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- IMPlications of IMP2 in RNA Biology and Disease.International journal of molecular sciences · 2025Review
- METTL3-modified exosomes from adipose-derived stem cells enhance the proliferation and migration of dermal fibroblasts by mediating m6A modification of CCNB1 mRNA.Archives of dermatological research · 2025Article
- Epigenetic orchestration of RNA mInternational journal of biological sciences · 2025Review
- METTL3-Mediated mDiabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Mitochondrial dysfunction in diabetic ulcers: pathophysiological mechanisms and targeted therapeutic strategies.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundDiabetic foot ulcer (DFU) is the most devastating complication of diabetes mellitus (DM) and plays a major role in disability and death in DM patients. NADH: ubiquinone oxidoreductase subunit B5 (NDUFB5) plays an important role in maintaining mitochondrial respiration, but whether it is involved in regulating the progression of advanced glycation end products (AGEs)-mediated DFU is still unclear.
methodsFirstly, the role of AGEs on cell viability, migration, and mitochondrial respiration in human umbilical vein endothelial cells (HUVECs) was explored in vitro. Next, NDUFB5 expression was detected in human samples and AGEs-treated HUVECs, and NDUFB5's effect on AGEs-induced HUVECs injury and skin wound in diabetic mice was further clarified. In addition, the role of m6A modification mediated by methyltransferase-like 3 (METTL3) in regulating NDUFB5 expression and AGEs-induced HUVECs injury was investigated.
resultsNDUFB5 promoted cell viability, migration, and mitochondrial respiration in AGEs-treated HUVECs, whereas mitochondrial fusion promoter M1 facilitated cell viability, migration, and mitochondrial oxiadative respiration in NDUFB5 knockdown HUVECs. Meanwhile, NDUFB5 promotes skin wound healing in diabetic mice. Besides, METTL3-mediated m6A modification and insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) enhanced NDUFB5 expression in HUVECs. Furthermore, METTL3 promoted cell viability, migration, and mitochondrial respiration in AGEs-treated HUVECs by increasing NDUFB5.
conclusionMETTL3-mediated NDUFB5 m6A modification inhibits AGEs-induced cell injury in HUVECs. METTL3 and NDUFB5 might serve as potential targets for DFU therapy in the future.
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