ArticleResearch (Washington, D.C.)2024
Diabetes Primes Neutrophils for Neutrophil Extracellular Trap Formation through Trained Immunity.
Article in Research (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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Who cites it
37 citing papers in PubMed, 31 citations in OpenAlex.
- Neutrophils: The Overlooked Regenerative Role in Bone Repair.Stem cell reviews and reports · 2026Review
- Review
- Bloodstream Infection After Major Burn Surgery in Relation to Preoperative Glycemic Gap Among Patients Without Diabetes: A Retrospective Cohort Study.International journal of molecular sciences · 2026Article
- Trained immunity: New insights into pathogenesis and therapeutic targets in diabetes and diabetic complications.Genes & diseases · 2026Review
- Fibrin formation and lysis in hyperglycaemia - molecular and cellular drivers.Current opinion in hematology · 2026Review
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Advances in Chinese herbal medicine for diabetic wound treatment: from tradition to innovation.Chinese medicine · 2026Review
- The diabetic wound microenvironment drives emergence and maintenance of CovRS variants in group BInfection and immunity · 2026Article
- Trained Immunity in Neutrophils and Mononuclear Phagocytes: Mechanisms and Pathophysiological Functions.Cells · 2026Review
- Trained Immunity in Autoimmunity: Friend, Foe, or Therapeutic Target?Biomedicines · 2026Article
- Review
- Biomaterial regulation of excessive inflammation restores osteoimmune homeostasis in diabetic bone regeneration.Regenerative biomaterials · 2026Review
- PANoptosis in diabetic retinopathy: immunological insights into mechanisms and translational therapies.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in antifungal immunity: mechanisms, dual roles, regulatory networks, and clinical perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Neutrophil extracellular traps in diabetic wound healing: mechanisms, pathological roles, and therapeutic implications.Burns & trauma · 2026Review
- The Paradox of NET Involvement in the Pathogenesis of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2026Review
- Directing Neutrophil Fate via Sensory-Immune Interactions Accelerates Diabetic Bone Healing.Research (Washington, D.C.) · 2026Article
- Global genome analysis identifies glycolipids and lipoteichoic acid alanylation as contributors to group B streptococcal diabetic wound infection.Cell reports · 2025Article
- The miR-3164/PAD4 axis regulates NETosis to prevent airway inflammation and remodeling through the TLR2/NF-κB signaling pathway.European journal of medical research · 2025Article
- Live fast, die young: neutrophils streamline their metabolism to maximize inflammation.Infection and immunity · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are primed for neutrophil extracellular trap (NET) formation during diabetes, and excessive NET formation from primed neutrophils compromises wound healing in patients with diabetes. Here, we demonstrate that trained immunity mediates diabetes-induced NET priming in neutrophils. Under diabetic conditions, neutrophils exhibit robust metabolic reprogramming comprising enhanced glycolysis via the pentose phosphate pathway and fatty acid oxidation, which result in the accumulation of acetyl-coenzyme A. Adenosine 5'-triphosphate-citrate lyase-mediated accumulation of acetyl-coenzyme A and histone acetyltransferases further induce the acetylation of lysine residues on histone 3 (AcH3K9, AcH3K14, and AcH3K27) and histone 4 (AcH4K8). The pharmacological inhibition of adenosine 5'-triphosphate-citrate lyase and histone acetyltransferases completely inhibited high-glucose-induced NET priming. The trained immunity of neutrophils was further confirmed in neutrophils isolated from patients with diabetes. Our findings suggest that trained immunity mediates functional changes in neutrophils in diabetic environments, and targeting neutrophil-trained immunity may be a potential therapeutic target for controlling inflammatory complications of diabetes.
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.