ArticleThe Journal of investigative dermatology2019
SIRT3 Regulates Macrophage-Mediated Inflammation in Diabetic Wound Repair.
Article in The Journal of investigative dermatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Loss of sirtuin 3 disrupts cellular senescence signaling pathways.GeroScience · 2026Article
- Observational
- Targeting SIRT3 dysfunction with a sprayable honokiol hydrogel for diabetic burn wound repair.Frontiers in pharmacology · 2026Article
- IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3.Nature communications · 2025Article
- Exosomes from adipose-derived stem cells: A potential therapeutic strategy for diabetic foot ulcers.World journal of diabetes · 2025Review
- SZC-6 Promotes Diabetic Wound Healing in Mice by Modulating the M1/M2 Macrophage Ratio and Inhibiting the MyD88/NF-χB Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Constructing a 3D co-cultureMaterials today. Bio · 2025Article
- Brown adipose tissue transplantation ameliorates hindlimb ischemic damage in diabetic mice.Scientific reports · 2025Article
- Frataxin deficiency and the pathology of Friedreich's Ataxia across tissues.Tissue barriers · 2025Review
- Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025Review
- The STAT3/SETDB2 axis dictates NF-κB-mediated inflammation in macrophages during wound repair.JCI insight · 2024Article
- Impacts of stem cells from different sources on wound healing rate in diabetic foot ulcers: a systematic review and meta-analysis.Frontiers in genetics · 2024Review
- Double cross-linked graphene oxide hydrogel for promoting healing of diabetic ulcers.Frontiers in chemistry · 2024Article
- Exosomal miR-4645-5p from hypoxic bone marrow mesenchymal stem cells facilitates diabetic wound healing by restoring keratinocyte autophagy.Burns & trauma · 2024Article
- Multifunctional Drugs-Loaded Carbomol Hydrogel Promotes Diabetic Wound Healing via Antimicrobial and Immunoregulation.Gels (Basel, Switzerland) · 2023Article
- Frataxin Deacetylation in Macrophages: Avoiding SIRTain Myocyte Death.Circulation research · 2023Article
- Preparation of Antibacterial, Arginine-Modified Ag Nanoclusters in the Hydrogel Used for Promoting Diabetic, Infected Wound Healing.ACS omega · 2023Article
- Function and mechanism of mesenchymal stem cells in the healing of diabetic foot wounds.Frontiers in endocrinology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Control of inflammation is critical for the treatment of nonhealing wounds, but a delicate balance exists between early inflammation that is essential for normal tissue repair and the pathologic inflammation that can occur later in the repair process. This necessitates the development of novel therapies that can target inflammation at the appropriate time during repair. Here, we found that SIRT3 is essential for normal healing and regulates inflammation in wound macrophages after injury. Under prediabetic conditions, SIRT3 was decreased in wound macrophages and resulted in dysregulated inflammation. In addition, we found that FABP4 regulates SIRT3 in human blood monocytes, and inhibition of FABP4 in wound macrophages decreases inflammatory cytokine expression, making FABP4 a viable target for the regulation of excess inflammation and wound repair in diabetes. Using a series of ex vivo and in vivo studies with genetically engineered mouse models and diabetic human monocytes, we showed that FABP4 expression is epigenetically upregulated in diabetic wound macrophages and, in turn, diminishes SIRT3 expression, thereby promoting inflammation. These findings have significant implications for controlling inflammation and promoting tissue repair in diabetic wounds.
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.