ArticleInflammation2016
Activation of α7nAChR Promotes Diabetic Wound Healing by Suppressing AGE-Induced TNF-α Production.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Natural Bioactive-Based Advanced Wound Dressings for Diabetic Wound Healing: A Systematic Review of Emerging Biomaterial Platforms.International journal of nanomedicine · 2026Pooled it
- Systematic review and meta-analysis of mouse models of diabetes-associated ulcers.BMJ open diabetes research & care · 2020Pooled it
- Parthenolide accelerates diabetic wound healing through the STAT3 and TNF-α/NF-kappaB pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Multi-target healing mechanisms ofAvicenna journal of phytomedicine · 2026Article
- Mitochondria-mediated inflammation and diabetic wound healing: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Dynamic C-reactive protein trajectories predict prolonged healing time in diabetic wounds: a machine learning model based on a single-center cohort with standardized wound size.Frontiers in medicine · 2026Article
- Article
- Polymers and Bioactive Compounds with a Macrophage Modulation Effect for the Rational Design of Hydrogels for Skin Regeneration.Pharmaceutics · 2023Article
- Neuroimmune nexus in the pathophysiology and therapy of inflammatory disorders: Role of α7 nicotinic acetylcholine receptors.Pharmacological research · 2023Review
- Sympathetic System in Wound Healing: Multistage Control in Normal and Diabetic Skin.International journal of molecular sciences · 2023Review
- Mechanisms of resveratrol against diabetic wound by network pharmacology and experimental validation.Annals of medicine · 2023Article
- Stereological and molecular studies on the effects of Ferula persica extract on wound healing in rats.Veterinary medicine and science · 2022Article
- Macrophage polarization in diabetic wound healing.Burns & trauma · 2022Review
- Heme oxygenase-1 alleviates advanced glycation end product-induced oxidative stress, inflammatory response and biological behavioral disorders in rat dermal fibroblasts.Experimental and therapeutic medicine · 2021Article
- Adrenomedullin 2 improves bone regeneration in type 1 diabetic rats by restoring imbalanced macrophage polarization and impaired osteogenesis.Stem cell research & therapy · 2021Article
- Targeted inhibition of endothelial calpain delays wound healing by reducing inflammation and angiogenesis.Cell death & disease · 2020Article
- Article
- Topical nicotinic receptor activation improves wound bacterial infection outcomes and TLR2-mediated inflammation in diabetic mouse wounds.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2018Article
- α7-nAChR Activation Has an Opposite Effect on Healing of Covered and Uncovered Wounds.Inflammation · 2018Article
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes frequently presents accumulation of advanced glycation end products (AGEs), which might induce excessive TNF-α production from macrophages to cause impaired wound healing. Recent studies have shown that activation of α7 nicotinic acetylcholine receptor (α7nAChR) on macrophages efficiently suppressed TNF-α synthesis. The aim of this study was to investigate the accumulation of AGEs in the wounds and determine whether PNU282987, an α7nAChR agonist, can improve wound repair by inhibiting AGE-mediated TNF-α production in a streptozotocin (STZ)-induced diabetic mouse model. Animals were assigned into four groups: wounded control group, wounded diabetic group, wounded diabetic group treated intraperitoneally with PNU282987, or wounded diabetic group treated intraperitoneally with vehicle. Compared with the non-diabetic control mice, the diabetic mice exhibited delayed wound healing that was characterized by elevated accumulation of AGEs, increased TNF-α level and macrophage infiltration, and decreased fibroblast number and collagen deposition at the late stage of repair. Besides, macrophages of diabetic wounds showed expression of α7nAChR. During late repair, PNU282987 treatment of diabetic mice significantly reduced the level of TNF-α, accelerated wound healing, and elevated fibroblast number and collagen deposition. To investigate the cellular mechanism of these observations, RAW 264.7 cells, a macrophage cell line, were incubated with AGEs in the presence or absence of PNU282987. TNF-α production from AGE-stimulated macrophages was significantly decreased by PNU282987 in a dose-dependent manner. Furthermore, PNU282987 significantly inhibited AGE-induced nuclear factor-κB (NF-κB) activation and receptor for AGE (RAGE) expression. These results strongly suggest that activating α7nAChR can promote diabetic wound healing by suppressing AGE-induced TNF-α production, which may be closely associated with the blockage of NF-κB activation in macrophages.
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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.