ArticleMolecular medicine (Cambridge, Mass.)2024
AMPK activation eliminates senescent cells in diabetic wound by inducing NCOA4 mediated ferritinophagy.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed.
- Article
- Astaxanthin-metformin conjugate nanomicelles-loaded hydrogel reprograms macrophage metabolismBioactive materials · 2026Article
- Crosstalk between autophagy and ferroptosis in diabetes.Genes & diseases · 2026Review
- Review
- Integrative Multiomics and Network Pharmacology Exploration of Active Components and Mechanisms of Action of Qufu Shengxin Ointment in Treating Chronic Nonhealing Wounds.Mediators of inflammation · 2026Article
- NCOA4 as a regulatory switch linking DNA damage to lipid peroxidation in radiation response.Frontiers in cell and developmental biology · 2026Review
- Autophagy-Ferroptosis Interplay Network: Redefining Therapeutic Paradigms for Diabetic Wound Healing.Journal of inflammation research · 2026Review
- Glucolipid metabolic disorders and ferroptosis in diabetic ulcers: pathogenic crossroads and therapeutic opportunities.Frontiers in endocrinology · 2026Review
- Autophagic degradation of SQSTM1 enables fibroblast activation to accelerate wound healing.Autophagy · 2025Article
- The protein phosphatase 6 subunit SAPS3 modulates lifespan by regulating metabolism.Science advances · 2025Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Extracellular vesicle-derived lncRNA VIM-AS1 promotes diabetic wound healing by promoting glycolysis and alleviating cellular senescence.Stem cell research & therapy · 2025Article
- Targeting Ferroptosis to Eliminate Senescent Cells: Mechanisms and Therapeutic Potential.Aging and disease · 2025Review
- Nuclear receptor coactive 4-mediated ferritinophagy: a key role of heavy metals toxicity.Archives of toxicology · 2025Review
- Ferroptosis: iron release mechanisms in the bioenergetic process.Cancer metastasis reviews · 2025Review
- Metabolism, senescence, and natural products: new perspectives on wound healing in diabetes.Frontiers in nutrition · 2025Review
- AMPK-ULK1-Mediated Ferritinophagy Drives Ferroptosis in GLA-Induced Testicular Toxicity.Research (Washington, D.C.) · 2025Article
- A nutrigeroscience approach: Dietary macronutrients and cellular senescence.Cell metabolism · 2024Review
- Clearance of senescent cells enhances skin wound healing in type 2 diabetic mice.Theranostics · 2024Article
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8 authors.
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Abstract
backgroundDiabetic wounds are one of the long-term complications of diabetes, with a disordered microenvironment, diabetic wounds can easily develop into chronic non-healing wounds, which can impose a significant burden on healthcare. In diabetic condition, senescent cells accumulate in the wound area and suppress the wound healing process. AMPK, as a molecule related to metabolism, has a close relationship with aging and diabetes. The purpose of this study was to investigate the effects of AMPK activation on wound healing and explore the underlying mechanisms.
methodsAMPK activator A769662 was topically applied in wound models of diabetic mice. Alterations in the wound site were observed and analyzed by immunohistochemistry. The markers related to autophagy and ferritinophagy were analyzed by western blotting and immunofluorescence staining. The role of AMPK activation and ferritinophagy were also analyzed by western blotting.
resultsOur results show that AMPK activation improved diabetic wound healing and reduced the accumulation of senescent cells. Intriguingly, we found that AMPK activation-induced ferroptosis is autophagy-dependent. We detected that the level of ferritin had deceased and NCOA4 was markedly increased after AMPK activation treatment. We further investigated that NCOA4-mediated ferritinophagy was involved in ferroptosis triggered by AMPK activation. Most importantly, AMPK activation can reverse the ferroptosis-insensitive of senescent fibroblast cells in diabetic mice wound area and promote wound healing.
conclusionsThese results suggest that activating AMPK can promote diabetic wound healing by reversing the ferroptosis-insensitive of senescent fibroblast cells. AMPK may serve as a regulatory factor in senescent cells in the diabetic wound area, therefore AMPK activation can become a promising therapeutic method for diabetic non-healing wounds.
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